Ignet

Gene Information

Gene symbol: STAT5B

Gene name: signal transducer and activator of transcription 5B

HGNC ID: 11367

Related Genes

#	Gene Symbol	Number of hits
1	ADIPOQ	1 hits
2	BCL2L1	1 hits
3	BMP2	1 hits
4	BTK	1 hits
5	C2orf28	1 hits
6	CD4	1 hits
7	CD8A	1 hits
8	CDKN1A	1 hits
9	CDKN2A	1 hits
10	CDKN2B	1 hits
11	CRKL	1 hits
12	CSF2	1 hits
13	EPO	1 hits
14	ESR1	1 hits
15	FOXM1	1 hits
16	FOXP3	1 hits
17	GHR	1 hits
18	GORASP1	1 hits
19	IGF1	1 hits
20	IL10	1 hits
21	IL2	1 hits
22	IL2RA	1 hits
23	IL2RB	1 hits
24	INS	1 hits
25	JAK2	1 hits
26	LEP	1 hits
27	MAPK1	1 hits
28	MAPK3	1 hits
29	NFKB1	1 hits
30	PIK3R1	1 hits
31	PIM1	1 hits
32	PPARG	1 hits
33	PRL	1 hits
34	PRLR	1 hits
35	PTPN11	1 hits
36	RACGAP1	1 hits
37	RASA1	1 hits
38	SH2D1A	1 hits
39	SOCS3	1 hits
40	STAT1	1 hits
41	STAT3	1 hits
42	STAT5A	1 hits
43	ZAP70	1 hits

Related Sentences

#	PMID	Sentence
1	7568026	Cloning and expression of Stat5 and an additional homologue (Stat5b) involved in prolactin signal transduction in mouse mammary tissue.
2	7568026	Prolactin (PRL) induces transcriptional activation of milk protein genes, such as the whey acidic protein (WAP), beta-casein, and beta-lactoglobulin genes, through a signaling cascade encompassing the Janus kinase Jak2 and the mammary gland factor (MGF; also called Stat5), which belongs to the family of proteins of signal transducers and activators of transcription (STAT).
3	7568026	We isolated and sequenced from mouse mammary tissue Stat5 mRNA and a previously unreported member, which we named Stat5b (Stat5 is renamed to Stat5a).
4	7568026	On the protein level Stat5a and Stat5b show a 96% sequence similarity.
5	7568026	Both Stat5a and Stat5b recognized the GAS site (gamma-interferon-activating sequence; TTCNNNGAA) in vitro and mediated PRL-induced transcription in COS cells transfected with a PRL receptor.
6	7568026	Stat5b also induced basal transcription in the absence of PRL.
7	7568026	Similar levels of Stat5a and Stat5b mRNAs were found in most tissues of virgin and lactating mice, but a differential accumulation of the Stat5 mRNAs was found in muscle and mammary tissue.
8	7568026	Cloning and expression of Stat5 and an additional homologue (Stat5b) involved in prolactin signal transduction in mouse mammary tissue.
9	7568026	Prolactin (PRL) induces transcriptional activation of milk protein genes, such as the whey acidic protein (WAP), beta-casein, and beta-lactoglobulin genes, through a signaling cascade encompassing the Janus kinase Jak2 and the mammary gland factor (MGF; also called Stat5), which belongs to the family of proteins of signal transducers and activators of transcription (STAT).
10	7568026	We isolated and sequenced from mouse mammary tissue Stat5 mRNA and a previously unreported member, which we named Stat5b (Stat5 is renamed to Stat5a).
11	7568026	On the protein level Stat5a and Stat5b show a 96% sequence similarity.
12	7568026	Both Stat5a and Stat5b recognized the GAS site (gamma-interferon-activating sequence; TTCNNNGAA) in vitro and mediated PRL-induced transcription in COS cells transfected with a PRL receptor.
13	7568026	Stat5b also induced basal transcription in the absence of PRL.
14	7568026	Similar levels of Stat5a and Stat5b mRNAs were found in most tissues of virgin and lactating mice, but a differential accumulation of the Stat5 mRNAs was found in muscle and mammary tissue.
15	7568026	Cloning and expression of Stat5 and an additional homologue (Stat5b) involved in prolactin signal transduction in mouse mammary tissue.
16	7568026	Prolactin (PRL) induces transcriptional activation of milk protein genes, such as the whey acidic protein (WAP), beta-casein, and beta-lactoglobulin genes, through a signaling cascade encompassing the Janus kinase Jak2 and the mammary gland factor (MGF; also called Stat5), which belongs to the family of proteins of signal transducers and activators of transcription (STAT).
17	7568026	We isolated and sequenced from mouse mammary tissue Stat5 mRNA and a previously unreported member, which we named Stat5b (Stat5 is renamed to Stat5a).
18	7568026	On the protein level Stat5a and Stat5b show a 96% sequence similarity.
19	7568026	Both Stat5a and Stat5b recognized the GAS site (gamma-interferon-activating sequence; TTCNNNGAA) in vitro and mediated PRL-induced transcription in COS cells transfected with a PRL receptor.
20	7568026	Stat5b also induced basal transcription in the absence of PRL.
21	7568026	Similar levels of Stat5a and Stat5b mRNAs were found in most tissues of virgin and lactating mice, but a differential accumulation of the Stat5 mRNAs was found in muscle and mammary tissue.
22	7568026	Cloning and expression of Stat5 and an additional homologue (Stat5b) involved in prolactin signal transduction in mouse mammary tissue.
23	7568026	Prolactin (PRL) induces transcriptional activation of milk protein genes, such as the whey acidic protein (WAP), beta-casein, and beta-lactoglobulin genes, through a signaling cascade encompassing the Janus kinase Jak2 and the mammary gland factor (MGF; also called Stat5), which belongs to the family of proteins of signal transducers and activators of transcription (STAT).
24	7568026	We isolated and sequenced from mouse mammary tissue Stat5 mRNA and a previously unreported member, which we named Stat5b (Stat5 is renamed to Stat5a).
25	7568026	On the protein level Stat5a and Stat5b show a 96% sequence similarity.
26	7568026	Both Stat5a and Stat5b recognized the GAS site (gamma-interferon-activating sequence; TTCNNNGAA) in vitro and mediated PRL-induced transcription in COS cells transfected with a PRL receptor.
27	7568026	Stat5b also induced basal transcription in the absence of PRL.
28	7568026	Similar levels of Stat5a and Stat5b mRNAs were found in most tissues of virgin and lactating mice, but a differential accumulation of the Stat5 mRNAs was found in muscle and mammary tissue.
29	7568026	Cloning and expression of Stat5 and an additional homologue (Stat5b) involved in prolactin signal transduction in mouse mammary tissue.
30	7568026	Prolactin (PRL) induces transcriptional activation of milk protein genes, such as the whey acidic protein (WAP), beta-casein, and beta-lactoglobulin genes, through a signaling cascade encompassing the Janus kinase Jak2 and the mammary gland factor (MGF; also called Stat5), which belongs to the family of proteins of signal transducers and activators of transcription (STAT).
31	7568026	We isolated and sequenced from mouse mammary tissue Stat5 mRNA and a previously unreported member, which we named Stat5b (Stat5 is renamed to Stat5a).
32	7568026	On the protein level Stat5a and Stat5b show a 96% sequence similarity.
33	7568026	Both Stat5a and Stat5b recognized the GAS site (gamma-interferon-activating sequence; TTCNNNGAA) in vitro and mediated PRL-induced transcription in COS cells transfected with a PRL receptor.
34	7568026	Stat5b also induced basal transcription in the absence of PRL.
35	7568026	Similar levels of Stat5a and Stat5b mRNAs were found in most tissues of virgin and lactating mice, but a differential accumulation of the Stat5 mRNAs was found in muscle and mammary tissue.
36	7568026	Cloning and expression of Stat5 and an additional homologue (Stat5b) involved in prolactin signal transduction in mouse mammary tissue.
37	7568026	Prolactin (PRL) induces transcriptional activation of milk protein genes, such as the whey acidic protein (WAP), beta-casein, and beta-lactoglobulin genes, through a signaling cascade encompassing the Janus kinase Jak2 and the mammary gland factor (MGF; also called Stat5), which belongs to the family of proteins of signal transducers and activators of transcription (STAT).
38	7568026	We isolated and sequenced from mouse mammary tissue Stat5 mRNA and a previously unreported member, which we named Stat5b (Stat5 is renamed to Stat5a).
39	7568026	On the protein level Stat5a and Stat5b show a 96% sequence similarity.
40	7568026	Both Stat5a and Stat5b recognized the GAS site (gamma-interferon-activating sequence; TTCNNNGAA) in vitro and mediated PRL-induced transcription in COS cells transfected with a PRL receptor.
41	7568026	Stat5b also induced basal transcription in the absence of PRL.
42	7568026	Similar levels of Stat5a and Stat5b mRNAs were found in most tissues of virgin and lactating mice, but a differential accumulation of the Stat5 mRNAs was found in muscle and mammary tissue.
43	8961260	Activation of Stat5a and Stat5b by tyrosine phosphorylation is tightly linked to mammary gland differentiation.
44	8961260	Signal transducer and activator of transcription (Stat)5 was originally identified as a mammary gland factor (MGF) that binds to promoter sequences of milk protein genes and activates their transcription.
45	8961260	We have generated isoform-specific antibodies against Stat5a or Stat5b and show that both isoforms are present in similar amounts at the protein level in mammary tissues of virgin, pregnant, lactating, and involuting mice.
46	8961260	Upon phosphorylation, Stat5a and Stat5b form homo- and heterodimers.
47	8961260	Using electrophoretic mobility shift assay and supershift analysis, we demonstrated that the DNA-binding activity detected during lactation is composed of both Stat5a and Stat5b, but not of other STATs.
48	8961260	Activation of Stat5a and Stat5b by tyrosine phosphorylation is tightly linked to mammary gland differentiation.
49	8961260	Signal transducer and activator of transcription (Stat)5 was originally identified as a mammary gland factor (MGF) that binds to promoter sequences of milk protein genes and activates their transcription.
50	8961260	We have generated isoform-specific antibodies against Stat5a or Stat5b and show that both isoforms are present in similar amounts at the protein level in mammary tissues of virgin, pregnant, lactating, and involuting mice.
51	8961260	Upon phosphorylation, Stat5a and Stat5b form homo- and heterodimers.
52	8961260	Using electrophoretic mobility shift assay and supershift analysis, we demonstrated that the DNA-binding activity detected during lactation is composed of both Stat5a and Stat5b, but not of other STATs.
53	8961260	Activation of Stat5a and Stat5b by tyrosine phosphorylation is tightly linked to mammary gland differentiation.
54	8961260	Signal transducer and activator of transcription (Stat)5 was originally identified as a mammary gland factor (MGF) that binds to promoter sequences of milk protein genes and activates their transcription.
55	8961260	We have generated isoform-specific antibodies against Stat5a or Stat5b and show that both isoforms are present in similar amounts at the protein level in mammary tissues of virgin, pregnant, lactating, and involuting mice.
56	8961260	Upon phosphorylation, Stat5a and Stat5b form homo- and heterodimers.
57	8961260	Using electrophoretic mobility shift assay and supershift analysis, we demonstrated that the DNA-binding activity detected during lactation is composed of both Stat5a and Stat5b, but not of other STATs.
58	8961260	Activation of Stat5a and Stat5b by tyrosine phosphorylation is tightly linked to mammary gland differentiation.
59	8961260	Signal transducer and activator of transcription (Stat)5 was originally identified as a mammary gland factor (MGF) that binds to promoter sequences of milk protein genes and activates their transcription.
60	8961260	We have generated isoform-specific antibodies against Stat5a or Stat5b and show that both isoforms are present in similar amounts at the protein level in mammary tissues of virgin, pregnant, lactating, and involuting mice.
61	8961260	Upon phosphorylation, Stat5a and Stat5b form homo- and heterodimers.
62	8961260	Using electrophoretic mobility shift assay and supershift analysis, we demonstrated that the DNA-binding activity detected during lactation is composed of both Stat5a and Stat5b, but not of other STATs.
63	9009201	Binding of PRL to its receptor leads to the phosphorylation and activation of STAT (signal transducers and activators of transcription) proteins, which in turn promote the expression of specific genes.
64	9009201	The activity pattern of two STAT proteins, Stat5a and Stat5b, in mammary tissue during pregnancy suggests an active role for these transcription factors in epithelial cell differentiation and milk protein gene expression.
65	9009201	Although Stat5b has a 96% similarity with Stat5a and a superimposable expression pattern during mammary gland development it failed to counterbalance for the absence of Stat5a.
66	9009201	Binding of PRL to its receptor leads to the phosphorylation and activation of STAT (signal transducers and activators of transcription) proteins, which in turn promote the expression of specific genes.
67	9009201	The activity pattern of two STAT proteins, Stat5a and Stat5b, in mammary tissue during pregnancy suggests an active role for these transcription factors in epithelial cell differentiation and milk protein gene expression.
68	9009201	Although Stat5b has a 96% similarity with Stat5a and a superimposable expression pattern during mammary gland development it failed to counterbalance for the absence of Stat5a.
69	9605930	Binding of STAT5a and STAT5b to a single element resembling a gamma-interferon-activated sequence mediates the growth hormone induction of the mouse acid-labile subunit promoter in liver cells.
70	9605930	After birth, the endocrine actions of insulin-like growth factor (IGF)-I and -II become increasingly important.
71	9605930	In postnatal animals, most of circulating IGFs occur in 150-kDa complexes formed by association of an acid-labile subunit (ALS) with complexes of IGF and IGF-binding protein-3.
72	9605930	To map the GH response element, a series of 5'-deletion fragments of the mouse ALS promoter (nt -2001 to -49, A(+1)TG) were inserted in the luciferase reporter plasmid pGL3 and transfected into the H4-II-E rat hepatoma cell line.
73	9605930	Using antibodies directed against members of the family of signal transducers and activators of transcription (STAT), this complex was shown to be composed of STAT5a and STAT5b.
74	9605930	Thus, the transcriptional activation of the mouse ALS gene by GH is mediated by the binding of STAT5 isoforms to a single GAS-like element.
75	9605930	Binding of STAT5a and STAT5b to a single element resembling a gamma-interferon-activated sequence mediates the growth hormone induction of the mouse acid-labile subunit promoter in liver cells.
76	9605930	After birth, the endocrine actions of insulin-like growth factor (IGF)-I and -II become increasingly important.
77	9605930	In postnatal animals, most of circulating IGFs occur in 150-kDa complexes formed by association of an acid-labile subunit (ALS) with complexes of IGF and IGF-binding protein-3.
78	9605930	To map the GH response element, a series of 5'-deletion fragments of the mouse ALS promoter (nt -2001 to -49, A(+1)TG) were inserted in the luciferase reporter plasmid pGL3 and transfected into the H4-II-E rat hepatoma cell line.
79	9605930	Using antibodies directed against members of the family of signal transducers and activators of transcription (STAT), this complex was shown to be composed of STAT5a and STAT5b.
80	9605930	Thus, the transcriptional activation of the mouse ALS gene by GH is mediated by the binding of STAT5 isoforms to a single GAS-like element.
81	9887329	Molecular analysis revealed that expression of the mutant receptor caused the activation of Stat1, Stat5a and Stat5b, and the up-regulation of p16, p18 and p19 cell cycle inhibitors, leading to dramatic expansion of the resting zone of chondrocytes at the expense of the proliferating chondrocytes.
82	10224108	Insulin inhibits growth hormone signaling via the growth hormone receptor/JAK2/STAT5B pathway.
83	10224108	Insulin deficiency results in a decrease in liver GH receptor (GHR) expression, which can be reversed by insulin administration.
84	10224108	In osteoblasts, continuous insulin treatment decreases the fraction of cellular GHR localized to the plasma membrane.
85	10224108	Our present studies suggest that insulin treatment of hepatoma cells results in a time-dependent inhibition of acute GH-induced phosphorylation of STAT5B.
86	10224108	Whereas total protein levels of JAK2 were not reduced after insulin pretreatment for 16 h, GH-induced JAK2 phosphorylation was inhibited.
87	10224108	There was a concomitant decrease in GH binding and a reduction in immunoreactive GHR levels following pretreatment with insulin for 8-24 h.
88	10224108	In summary, continuous insulin treatment in rat H4 hepatoma cells reduces GH binding, immunoreactive GHR, GH-induced phosphorylation of JAK2, and GH-induced tyrosine phosphorylation of STAT5B.
89	10224108	Insulin inhibits growth hormone signaling via the growth hormone receptor/JAK2/STAT5B pathway.
90	10224108	Insulin deficiency results in a decrease in liver GH receptor (GHR) expression, which can be reversed by insulin administration.
91	10224108	In osteoblasts, continuous insulin treatment decreases the fraction of cellular GHR localized to the plasma membrane.
92	10224108	Our present studies suggest that insulin treatment of hepatoma cells results in a time-dependent inhibition of acute GH-induced phosphorylation of STAT5B.
93	10224108	Whereas total protein levels of JAK2 were not reduced after insulin pretreatment for 16 h, GH-induced JAK2 phosphorylation was inhibited.
94	10224108	There was a concomitant decrease in GH binding and a reduction in immunoreactive GHR levels following pretreatment with insulin for 8-24 h.
95	10224108	In summary, continuous insulin treatment in rat H4 hepatoma cells reduces GH binding, immunoreactive GHR, GH-induced phosphorylation of JAK2, and GH-induced tyrosine phosphorylation of STAT5B.
96	10224108	Insulin inhibits growth hormone signaling via the growth hormone receptor/JAK2/STAT5B pathway.
97	10224108	Insulin deficiency results in a decrease in liver GH receptor (GHR) expression, which can be reversed by insulin administration.
98	10224108	In osteoblasts, continuous insulin treatment decreases the fraction of cellular GHR localized to the plasma membrane.
99	10224108	Our present studies suggest that insulin treatment of hepatoma cells results in a time-dependent inhibition of acute GH-induced phosphorylation of STAT5B.
100	10224108	Whereas total protein levels of JAK2 were not reduced after insulin pretreatment for 16 h, GH-induced JAK2 phosphorylation was inhibited.
101	10224108	There was a concomitant decrease in GH binding and a reduction in immunoreactive GHR levels following pretreatment with insulin for 8-24 h.
102	10224108	In summary, continuous insulin treatment in rat H4 hepatoma cells reduces GH binding, immunoreactive GHR, GH-induced phosphorylation of JAK2, and GH-induced tyrosine phosphorylation of STAT5B.
103	10908145	The transcription factor Stat5a critically mediates prolactin (PRL)-induced mammary gland development and lactogenesis.
104	10908145	Serum testosterone and PRL levels were normal in Stat5a knockout mice, but prostate PRL receptor expression was reduced as determined by immunohistochemistry.
105	10908145	Expression levels or activation states of other PRL signal transduction proteins, including Stat5b, Stat3, Stat1, ERK1, and ERK2 were not altered.
106	11735219	In the mouse, STAT3, STAT5a, and STAT5b are encoded by adjacent genes on chromosome 11 (60.5 cM).
107	11735219	We identified six known genes and cloned two new genes, termed D11Lgp1 and D11Lgp2.
108	11781356	Diabetic LDL inhibits cell-cycle progression via STAT5B and p21(waf).
109	11781356	To dissect the molecular mechanisms of this effect, we analyzed the expression and function of the cyclin-dependent kinase inhibitor p21(waf), a cell cycle regulator known to be a target of the signal transducers and activators of transcription (STATs). dm-LDL led to transient STAT5 phosphorylation and the formation of a STAT5-containing complex and activated p21(waf) expression at the transcriptional level.
110	11781356	Expression of the dominant-negative form of STAT5B, but not of STAT5A, significantly decreased both p21(waf) expression and the fraction of cells in G1.
111	11781356	Diabetic LDL inhibits cell-cycle progression via STAT5B and p21(waf).
112	11781356	To dissect the molecular mechanisms of this effect, we analyzed the expression and function of the cyclin-dependent kinase inhibitor p21(waf), a cell cycle regulator known to be a target of the signal transducers and activators of transcription (STATs). dm-LDL led to transient STAT5 phosphorylation and the formation of a STAT5-containing complex and activated p21(waf) expression at the transcriptional level.
113	11781356	Expression of the dominant-negative form of STAT5B, but not of STAT5A, significantly decreased both p21(waf) expression and the fraction of cells in G1.
114	12540601	STAT5A promotes adipogenesis in nonprecursor cells and associates with the glucocorticoid receptor during adipocyte differentiation.
115	12540601	The differentiation of adipocytes is regulated by the activity of a variety of transcription factors, including peroxidase proliferator-activated receptor (PPAR)-gamma and C/EBPalpha.
116	12540601	Our current study demonstrates that ectopic expression of STAT5A, such as that of PPAR-gamma and C/EBPalpha, promotes adipogenesis in two nonprecursor fibroblast cell lines.
117	12540601	Using morphologic and biochemical criteria, we have demonstrated that STAT5A and the combination of STAT5A and STAT5B are sufficient to induce the expression of early and late adipogenic markers in BALB/c and NIH-3T3 cells.
118	12540601	Yet, the ectopic expression of STAT5B alone does not induce the expression of adipocyte genes, but enhances the induction of these genes in cells also expressing STAT5A.
119	12540601	This finding suggests that STAT5A and STAT5B do not function identically in adipocytes.
120	12540601	Moreover, we have shown that STAT5A is associated with the glucocorticoid receptor during adipogenesis in a highly regulated manner.
121	12540601	STAT5A promotes adipogenesis in nonprecursor cells and associates with the glucocorticoid receptor during adipocyte differentiation.
122	12540601	The differentiation of adipocytes is regulated by the activity of a variety of transcription factors, including peroxidase proliferator-activated receptor (PPAR)-gamma and C/EBPalpha.
123	12540601	Our current study demonstrates that ectopic expression of STAT5A, such as that of PPAR-gamma and C/EBPalpha, promotes adipogenesis in two nonprecursor fibroblast cell lines.
124	12540601	Using morphologic and biochemical criteria, we have demonstrated that STAT5A and the combination of STAT5A and STAT5B are sufficient to induce the expression of early and late adipogenic markers in BALB/c and NIH-3T3 cells.
125	12540601	Yet, the ectopic expression of STAT5B alone does not induce the expression of adipocyte genes, but enhances the induction of these genes in cells also expressing STAT5A.
126	12540601	This finding suggests that STAT5A and STAT5B do not function identically in adipocytes.
127	12540601	Moreover, we have shown that STAT5A is associated with the glucocorticoid receptor during adipogenesis in a highly regulated manner.
128	12540601	STAT5A promotes adipogenesis in nonprecursor cells and associates with the glucocorticoid receptor during adipocyte differentiation.
129	12540601	The differentiation of adipocytes is regulated by the activity of a variety of transcription factors, including peroxidase proliferator-activated receptor (PPAR)-gamma and C/EBPalpha.
130	12540601	Our current study demonstrates that ectopic expression of STAT5A, such as that of PPAR-gamma and C/EBPalpha, promotes adipogenesis in two nonprecursor fibroblast cell lines.
131	12540601	Using morphologic and biochemical criteria, we have demonstrated that STAT5A and the combination of STAT5A and STAT5B are sufficient to induce the expression of early and late adipogenic markers in BALB/c and NIH-3T3 cells.
132	12540601	Yet, the ectopic expression of STAT5B alone does not induce the expression of adipocyte genes, but enhances the induction of these genes in cells also expressing STAT5A.
133	12540601	This finding suggests that STAT5A and STAT5B do not function identically in adipocytes.
134	12540601	Moreover, we have shown that STAT5A is associated with the glucocorticoid receptor during adipogenesis in a highly regulated manner.
135	12588773	A functional polymorphism in a STAT5B site of the human PPAR gamma 3 gene promoter affects height and lipid metabolism in a French population.
136	14701862	The inapt transcriptional regulation ability of the mutated Stat5b is proved by decreased levels of RNA of Stat5b-regulated genes (IL-2Rbeta and Pim1).
137	14701862	Consequently, IL-2Rbeta and Pim1 proteins were shown by Western blotting to have lower levels in NOD compared with normal B6 mice.
138	15749807	Prolonged insulin treatment inhibits GH signaling via STAT3 and STAT1.
139	15749807	Previous studies in our laboratory have shown that GH induction of signal transducers and activators of transcription (STAT)5B tyrosine phosphorylation is inhibited by prolonged insulin treatment, probably via downregulation of GHR.
140	15749807	Here, we find that in rat H4IIE hepatoma cells GH-induced tyrosine phosphorylation of two other STATs (STAT3 and STAT1) was also greatly reduced following prolonged insulin pretreatment compared with that induced by GH alone.
141	15749807	In the present work, total STAT5B and STAT1 protein levels were not altered by prolonged insulin treatment.
142	15749807	However, prolonged insulin treatment (16 h; 10 or 100 nM) resulted in a 30-40% reduction of total STAT3 protein, with little change at 0.1 and 1.0 nM insulin.
143	15749807	Thus, there is a selective reduction of total STAT3 protein levels by insulin, but only at high concentration of insulin.
144	15749807	Basal tyrosine phosphorylated (PY)-STAT3 was also significantly reduced by prolonged insulin treatment, and to a greater extent than total STAT3 protein levels.
145	15749807	The inhibitory effect of insulin on total STAT3 protein and basal PY-STAT3 levels was dependent on activation of the MEK-ERK pathway, rather than the PI3K pathway.
146	15749807	In contrast, the MEK-ERK pathway did not play a major role in insulin's inhibition of GH-induced PY-STAT3 and PY-STAT1.
147	15749807	The present studies indicate that prolonged hyperinsulinemia, such as that found in some obese patients or patients with Type 2 diabetes mellitus, may have profound effects on GH signaling via STAT3 and STAT1.
148	16177100	Nonobese diabetic mouse congenic analysis reveals chromosome 11 locus contributing to diabetes susceptibility, macrophage STAT5 dysfunction, and granulocyte-macrophage colony-stimulating factor overproduction.
149	16177100	Unstimulated monocytes of at-risk/type 1 diabetic humans and macrophages of the NOD mouse have markedly elevated autocrine GM-CSF production and persistent STAT5 phosphorylation.
150	16177100	We analyzed the relationship between GM-CSF production and persistent STAT5 phosphorylation in NOD macrophages using reciprocal congenic mouse strains containing either diabetes-susceptible NOD (B6.NODC11), or diabetes-resistant C57L (NOD.LC11) loci on chromosome 11.
151	16177100	These intervals contain the gene for GM-CSF (Csf2; 53.8 Mb) and those for STAT3, STAT5A, and STAT5B (Stat3, Stat5a, and Stat5b; 100.4-100.6 Mb).
152	16177100	High GM-CSF production and persistent STAT5 phosphorylation in unactivated NOD macrophages can be linked to a region (44.9-55.7 Mb) containing the Csf2 gene, but not the Stat3/5a/5b genes.
153	16306356	Inhibition of preproinsulin gene expression by leptin induction of suppressor of cytokine signaling 3 in pancreatic beta-cells.
154	16306356	Leptin inhibits insulin secretion and preproinsulin gene expression in pancreatic beta-cells, but signal transduction pathways and molecular mechanisms underlying this effect are poorly characterized.
155	16306356	Leptin stimulation led to janus kinase (JAK)2-dependent phosphorylation and nuclear translocation of the transcription factors signal transducer and activator of transcription (STAT)3 and STAT5b in INS-1 beta-cells.
156	16306356	Leptin also induced mRNA expression of the JAK-STAT inhibitor suppressor of cytokine signaling (SOCS)3 in INS-1 beta-cells and human pancreatic islets in vitro and in pancreatic islets of ob/ob mice in vivo.
157	16306356	Transcriptional activation of the rat SOCS3 promoter by leptin was observed with concomitant leptin-induced STAT3 and STAT5b DNA binding to specific promoter regions.
158	16306356	Unexpectedly, SOCS3 inhibited both basal and STAT3/5b-dependent rat preproinsulin 1 gene promoter activity in INS-1 cells.
159	16306356	These results suggest that SOCS3 represents a transcriptional inhibitor of preproinsulin gene expression, which is induced by leptin through JAK-STAT3/5b signaling in pancreatic beta-cells.
160	16306356	In conclusion, although SOCS3 is believed to be a negative feedback regulator of JAK-STAT signaling, our findings suggest involvement of SOCS3 in a direct gene regulatory pathway downstream of leptin-activated JAK-STAT signaling in pancreatic beta-cells.
161	16306356	Inhibition of preproinsulin gene expression by leptin induction of suppressor of cytokine signaling 3 in pancreatic beta-cells.
162	16306356	Leptin inhibits insulin secretion and preproinsulin gene expression in pancreatic beta-cells, but signal transduction pathways and molecular mechanisms underlying this effect are poorly characterized.
163	16306356	Leptin stimulation led to janus kinase (JAK)2-dependent phosphorylation and nuclear translocation of the transcription factors signal transducer and activator of transcription (STAT)3 and STAT5b in INS-1 beta-cells.
164	16306356	Leptin also induced mRNA expression of the JAK-STAT inhibitor suppressor of cytokine signaling (SOCS)3 in INS-1 beta-cells and human pancreatic islets in vitro and in pancreatic islets of ob/ob mice in vivo.
165	16306356	Transcriptional activation of the rat SOCS3 promoter by leptin was observed with concomitant leptin-induced STAT3 and STAT5b DNA binding to specific promoter regions.
166	16306356	Unexpectedly, SOCS3 inhibited both basal and STAT3/5b-dependent rat preproinsulin 1 gene promoter activity in INS-1 cells.
167	16306356	These results suggest that SOCS3 represents a transcriptional inhibitor of preproinsulin gene expression, which is induced by leptin through JAK-STAT3/5b signaling in pancreatic beta-cells.
168	16306356	In conclusion, although SOCS3 is believed to be a negative feedback regulator of JAK-STAT signaling, our findings suggest involvement of SOCS3 in a direct gene regulatory pathway downstream of leptin-activated JAK-STAT signaling in pancreatic beta-cells.
169	16505237	Impaired Crkl expression contributes to the defective DNA binding of Stat5b in nonobese diabetic mice.
170	16505237	To our surprise, the binding ability of Stat5b is inconsistent with the presence or absence of the Stat5b mutation in these congenic mice but is correlated with the expression levels of the Crkl protein, which was coprecipitated by an anti-Stat5b antibody.
171	16505237	Both the expression of Crkl and the Stat5b binding ability are the highest in B6.NOD-c11 and the lowest in NOD while intermediate in B6 and NOD.Lc11 mice.
172	16505237	We demonstrated that the adapter molecule Crkl can bind Stat5b and that the Crkl protein is a Stat5b binding cofactor.
173	16505237	More importantly, profection of Crkl recombinant protein significantly increased Stat5b binding ability and rescued the binding defect of the NOD mutant Stat5b, suggesting that Crkl is a key regulatory molecule for Stat5b binding.
174	16505237	Therefore, the defective Crkl expression may contribute to the development of diabetes in the NOD mice by exacerbating the defective Stat5b binding ability.
175	16505237	Impaired Crkl expression contributes to the defective DNA binding of Stat5b in nonobese diabetic mice.
176	16505237	To our surprise, the binding ability of Stat5b is inconsistent with the presence or absence of the Stat5b mutation in these congenic mice but is correlated with the expression levels of the Crkl protein, which was coprecipitated by an anti-Stat5b antibody.
177	16505237	Both the expression of Crkl and the Stat5b binding ability are the highest in B6.NOD-c11 and the lowest in NOD while intermediate in B6 and NOD.Lc11 mice.
178	16505237	We demonstrated that the adapter molecule Crkl can bind Stat5b and that the Crkl protein is a Stat5b binding cofactor.
179	16505237	More importantly, profection of Crkl recombinant protein significantly increased Stat5b binding ability and rescued the binding defect of the NOD mutant Stat5b, suggesting that Crkl is a key regulatory molecule for Stat5b binding.
180	16505237	Therefore, the defective Crkl expression may contribute to the development of diabetes in the NOD mice by exacerbating the defective Stat5b binding ability.
181	16505237	Impaired Crkl expression contributes to the defective DNA binding of Stat5b in nonobese diabetic mice.
182	16505237	To our surprise, the binding ability of Stat5b is inconsistent with the presence or absence of the Stat5b mutation in these congenic mice but is correlated with the expression levels of the Crkl protein, which was coprecipitated by an anti-Stat5b antibody.
183	16505237	Both the expression of Crkl and the Stat5b binding ability are the highest in B6.NOD-c11 and the lowest in NOD while intermediate in B6 and NOD.Lc11 mice.
184	16505237	We demonstrated that the adapter molecule Crkl can bind Stat5b and that the Crkl protein is a Stat5b binding cofactor.
185	16505237	More importantly, profection of Crkl recombinant protein significantly increased Stat5b binding ability and rescued the binding defect of the NOD mutant Stat5b, suggesting that Crkl is a key regulatory molecule for Stat5b binding.
186	16505237	Therefore, the defective Crkl expression may contribute to the development of diabetes in the NOD mice by exacerbating the defective Stat5b binding ability.
187	16505237	Impaired Crkl expression contributes to the defective DNA binding of Stat5b in nonobese diabetic mice.
188	16505237	To our surprise, the binding ability of Stat5b is inconsistent with the presence or absence of the Stat5b mutation in these congenic mice but is correlated with the expression levels of the Crkl protein, which was coprecipitated by an anti-Stat5b antibody.
189	16505237	Both the expression of Crkl and the Stat5b binding ability are the highest in B6.NOD-c11 and the lowest in NOD while intermediate in B6 and NOD.Lc11 mice.
190	16505237	We demonstrated that the adapter molecule Crkl can bind Stat5b and that the Crkl protein is a Stat5b binding cofactor.
191	16505237	More importantly, profection of Crkl recombinant protein significantly increased Stat5b binding ability and rescued the binding defect of the NOD mutant Stat5b, suggesting that Crkl is a key regulatory molecule for Stat5b binding.
192	16505237	Therefore, the defective Crkl expression may contribute to the development of diabetes in the NOD mice by exacerbating the defective Stat5b binding ability.
193	16505237	Impaired Crkl expression contributes to the defective DNA binding of Stat5b in nonobese diabetic mice.
194	16505237	To our surprise, the binding ability of Stat5b is inconsistent with the presence or absence of the Stat5b mutation in these congenic mice but is correlated with the expression levels of the Crkl protein, which was coprecipitated by an anti-Stat5b antibody.
195	16505237	Both the expression of Crkl and the Stat5b binding ability are the highest in B6.NOD-c11 and the lowest in NOD while intermediate in B6 and NOD.Lc11 mice.
196	16505237	We demonstrated that the adapter molecule Crkl can bind Stat5b and that the Crkl protein is a Stat5b binding cofactor.
197	16505237	More importantly, profection of Crkl recombinant protein significantly increased Stat5b binding ability and rescued the binding defect of the NOD mutant Stat5b, suggesting that Crkl is a key regulatory molecule for Stat5b binding.
198	16505237	Therefore, the defective Crkl expression may contribute to the development of diabetes in the NOD mice by exacerbating the defective Stat5b binding ability.
199	16505237	Impaired Crkl expression contributes to the defective DNA binding of Stat5b in nonobese diabetic mice.
200	16505237	To our surprise, the binding ability of Stat5b is inconsistent with the presence or absence of the Stat5b mutation in these congenic mice but is correlated with the expression levels of the Crkl protein, which was coprecipitated by an anti-Stat5b antibody.
201	16505237	Both the expression of Crkl and the Stat5b binding ability are the highest in B6.NOD-c11 and the lowest in NOD while intermediate in B6 and NOD.Lc11 mice.
202	16505237	We demonstrated that the adapter molecule Crkl can bind Stat5b and that the Crkl protein is a Stat5b binding cofactor.
203	16505237	More importantly, profection of Crkl recombinant protein significantly increased Stat5b binding ability and rescued the binding defect of the NOD mutant Stat5b, suggesting that Crkl is a key regulatory molecule for Stat5b binding.
204	16505237	Therefore, the defective Crkl expression may contribute to the development of diabetes in the NOD mice by exacerbating the defective Stat5b binding ability.
205	16730240	The mRNA levels of three members of the family of signal transducers and activators of transcription, STAT1, STAT3 and STAT5b, were also increased 2-4 times.
206	17003334	Pancreatic beta-cell growth and survival and insulin production are stimulated by growth hormone and prolactin through activation of the transcription factor signal transducer and activator of transcription (STAT)5.
207	17003334	To assess the role of STAT5 activity in beta-cells in vivo, we generated transgenic mice that expressed a dominant-negative mutant of STAT5a (DNSTAT5) or constitutive active mutant of STAT5b (CASTAT5) under control of the rat insulin 1 promoter (RIP).
208	17003334	The inhibitory effect of high-fat diet or leptin on insulin secretion was diminished in isolated islets from RIP-DNSTAT5 mice compared with wild-type islets.
209	17130555	Upregulation of Foxp3 expression in mouse and human Treg is IL-2/STAT5 dependent: implications for the NOD STAT5B mutation in diabetes pathogenesis.
210	17130555	Regulatory T cells (Treg), characterized as CD4(+)/CD25(+hi) T cells, are critical for sustaining and promoting immune tolerance.
211	17130555	Based on the presence of five STAT5B consensus sequences in the Foxp3 promotor, we hypothesized a critical linkage between IL-2 signaling/STAT5B and Foxp3 expression in Treg.
212	17130555	Our data show IL-2 activates long-form (LF) STAT5 and sustains Foxp3 expression in Treg.
213	17130555	In contrast, CD4(+)/CD25(-) T cells do not active LF STAT5 and do not express Foxp3 under the same conditions.
214	17130555	Examination of human Treg using flow cytometry and intracellular staining for Foxp3 expression likewise demonstrates that IL-2 maintains Foxp3 expression through LF STAT5 signaling.
215	17130555	Upregulation of Foxp3 expression in mouse and human Treg is IL-2/STAT5 dependent: implications for the NOD STAT5B mutation in diabetes pathogenesis.
216	17130555	Regulatory T cells (Treg), characterized as CD4(+)/CD25(+hi) T cells, are critical for sustaining and promoting immune tolerance.
217	17130555	Based on the presence of five STAT5B consensus sequences in the Foxp3 promotor, we hypothesized a critical linkage between IL-2 signaling/STAT5B and Foxp3 expression in Treg.
218	17130555	Our data show IL-2 activates long-form (LF) STAT5 and sustains Foxp3 expression in Treg.
219	17130555	In contrast, CD4(+)/CD25(-) T cells do not active LF STAT5 and do not express Foxp3 under the same conditions.
220	17130555	Examination of human Treg using flow cytometry and intracellular staining for Foxp3 expression likewise demonstrates that IL-2 maintains Foxp3 expression through LF STAT5 signaling.
221	17130555	Upregulation of Foxp3 expression in mouse and human Treg is IL-2/STAT5 dependent: implications for the NOD STAT5B mutation in diabetes pathogenesis.
222	17130555	Regulatory T cells (Treg), characterized as CD4(+)/CD25(+hi) T cells, are critical for sustaining and promoting immune tolerance.
223	17130555	Based on the presence of five STAT5B consensus sequences in the Foxp3 promotor, we hypothesized a critical linkage between IL-2 signaling/STAT5B and Foxp3 expression in Treg.
224	17130555	Our data show IL-2 activates long-form (LF) STAT5 and sustains Foxp3 expression in Treg.
225	17130555	In contrast, CD4(+)/CD25(-) T cells do not active LF STAT5 and do not express Foxp3 under the same conditions.
226	17130555	Examination of human Treg using flow cytometry and intracellular staining for Foxp3 expression likewise demonstrates that IL-2 maintains Foxp3 expression through LF STAT5 signaling.
227	17130555	Upregulation of Foxp3 expression in mouse and human Treg is IL-2/STAT5 dependent: implications for the NOD STAT5B mutation in diabetes pathogenesis.
228	17130555	Regulatory T cells (Treg), characterized as CD4(+)/CD25(+hi) T cells, are critical for sustaining and promoting immune tolerance.
229	17130555	Based on the presence of five STAT5B consensus sequences in the Foxp3 promotor, we hypothesized a critical linkage between IL-2 signaling/STAT5B and Foxp3 expression in Treg.
230	17130555	Our data show IL-2 activates long-form (LF) STAT5 and sustains Foxp3 expression in Treg.
231	17130555	In contrast, CD4(+)/CD25(-) T cells do not active LF STAT5 and do not express Foxp3 under the same conditions.
232	17130555	Examination of human Treg using flow cytometry and intracellular staining for Foxp3 expression likewise demonstrates that IL-2 maintains Foxp3 expression through LF STAT5 signaling.
233	17130555	Upregulation of Foxp3 expression in mouse and human Treg is IL-2/STAT5 dependent: implications for the NOD STAT5B mutation in diabetes pathogenesis.
234	17130555	Regulatory T cells (Treg), characterized as CD4(+)/CD25(+hi) T cells, are critical for sustaining and promoting immune tolerance.
235	17130555	Based on the presence of five STAT5B consensus sequences in the Foxp3 promotor, we hypothesized a critical linkage between IL-2 signaling/STAT5B and Foxp3 expression in Treg.
236	17130555	Our data show IL-2 activates long-form (LF) STAT5 and sustains Foxp3 expression in Treg.
237	17130555	In contrast, CD4(+)/CD25(-) T cells do not active LF STAT5 and do not express Foxp3 under the same conditions.
238	17130555	Examination of human Treg using flow cytometry and intracellular staining for Foxp3 expression likewise demonstrates that IL-2 maintains Foxp3 expression through LF STAT5 signaling.
239	17158201	Postnatal body growth is dependent on the transcription factors signal transducers and activators of transcription 5a/b in muscle: a role for autocrine/paracrine insulin-like growth factor I.
240	17158201	The transcription factors signal transducers and activators of transcription (STAT)5a and STAT5b (STAT5) are essential mediators of many actions of GH, including transcription of the IGF-I gene.
241	17158201	Here, we present evidence that skeletal muscle STAT5 is important for postnatal growth and suggest that this is conveyed by the production of localized IGF-I.
242	17158201	To investigate the role of STAT5 signaling in skeletal muscle, mice with a skeletal-muscle-specific deletion of the Stat5a and Stat5b genes (Stat5MKO mice) were used.
243	17158201	These results demonstrate an as yet unreported critical role for STAT5 in skeletal muscle for local IGF-I production and postnatal growth and suggest the skeletal muscle as a major site of GH action.
244	17158201	Postnatal body growth is dependent on the transcription factors signal transducers and activators of transcription 5a/b in muscle: a role for autocrine/paracrine insulin-like growth factor I.
245	17158201	The transcription factors signal transducers and activators of transcription (STAT)5a and STAT5b (STAT5) are essential mediators of many actions of GH, including transcription of the IGF-I gene.
246	17158201	Here, we present evidence that skeletal muscle STAT5 is important for postnatal growth and suggest that this is conveyed by the production of localized IGF-I.
247	17158201	To investigate the role of STAT5 signaling in skeletal muscle, mice with a skeletal-muscle-specific deletion of the Stat5a and Stat5b genes (Stat5MKO mice) were used.
248	17158201	These results demonstrate an as yet unreported critical role for STAT5 in skeletal muscle for local IGF-I production and postnatal growth and suggest the skeletal muscle as a major site of GH action.
249	17158201	Postnatal body growth is dependent on the transcription factors signal transducers and activators of transcription 5a/b in muscle: a role for autocrine/paracrine insulin-like growth factor I.
250	17158201	The transcription factors signal transducers and activators of transcription (STAT)5a and STAT5b (STAT5) are essential mediators of many actions of GH, including transcription of the IGF-I gene.
251	17158201	Here, we present evidence that skeletal muscle STAT5 is important for postnatal growth and suggest that this is conveyed by the production of localized IGF-I.
252	17158201	To investigate the role of STAT5 signaling in skeletal muscle, mice with a skeletal-muscle-specific deletion of the Stat5a and Stat5b genes (Stat5MKO mice) were used.
253	17158201	These results demonstrate an as yet unreported critical role for STAT5 in skeletal muscle for local IGF-I production and postnatal growth and suggest the skeletal muscle as a major site of GH action.
254	17158201	Postnatal body growth is dependent on the transcription factors signal transducers and activators of transcription 5a/b in muscle: a role for autocrine/paracrine insulin-like growth factor I.
255	17158201	The transcription factors signal transducers and activators of transcription (STAT)5a and STAT5b (STAT5) are essential mediators of many actions of GH, including transcription of the IGF-I gene.
256	17158201	Here, we present evidence that skeletal muscle STAT5 is important for postnatal growth and suggest that this is conveyed by the production of localized IGF-I.
257	17158201	To investigate the role of STAT5 signaling in skeletal muscle, mice with a skeletal-muscle-specific deletion of the Stat5a and Stat5b genes (Stat5MKO mice) were used.
258	17158201	These results demonstrate an as yet unreported critical role for STAT5 in skeletal muscle for local IGF-I production and postnatal growth and suggest the skeletal muscle as a major site of GH action.
259	17367502	Stimulation of the PPARgamma by TZDs interferes with oestrogen receptor signalling, STAT5B and NF-kappaB signalling cascades.
260	17726024	The long form of the leptin receptor regulates STAT5 and ribosomal protein S6 via alternate mechanisms.
261	17726024	Here we demonstrate that leptin stimulates the phosphorylation of STAT5 and ribosomal protein S6 in the hypothalamic arcuate nucleus in mice.
262	17726024	Our analysis reveals a dominant role for LepRb Tyr(1077) (which we demonstrate to be phosphorylated during receptor activation) and a secondary role for LepRb Tyr(1138) in the acute phosphorylation of STAT5a and STAT5b.
263	17726024	In contrast, Tyr(985) (the LepRb phosphorylation site required for ERK activation) mediates the phosphorylation of the ribosomal S6 kinase (RSK) and S6, as well as cap-dependent translation.
264	18260110	Disease-causing mutations have been detected in the SH2 domains of cytoplasmic signaling proteins Bruton tyrosine kinase (BTK), SH2D1A, Ras GTPase activating protein (RasGAP), ZAP-70, SHP-2, STAT1, STAT5B, and the p85alpha subunit of the PIP3.
265	18260110	Mutations in the BTK, SH2D1A, ZAP70, STAT1, and STAT5B genes have been shown to cause diverse immunodeficiencies, whereas the mutations in RASA1 and PIK3R1 genes lead to basal carcinoma and diabetes, respectively.
266	18260110	Disease-causing mutations have been detected in the SH2 domains of cytoplasmic signaling proteins Bruton tyrosine kinase (BTK), SH2D1A, Ras GTPase activating protein (RasGAP), ZAP-70, SHP-2, STAT1, STAT5B, and the p85alpha subunit of the PIP3.
267	18260110	Mutations in the BTK, SH2D1A, ZAP70, STAT1, and STAT5B genes have been shown to cause diverse immunodeficiencies, whereas the mutations in RASA1 and PIK3R1 genes lead to basal carcinoma and diabetes, respectively.
268	18286195	STAT5A and STAT5B (STAT5), the most promiscuous members of this family, are highly expressed in specific populations of hypothalamic neurons in regions known to mediate the actions of cytokines in the regulation of energy balance.
269	18286195	Furthermore, central administration of GM-CSF mediated the nuclear accumulation of STAT5 in hypothalamic neurons and reduced food intake in control but not in mutant mice.
270	18286195	These results demonstrate that STAT5 mediates energy homeostasis in response to endogenous cytokines such as GM-CSF.
271	18347089	Interpretation of cytokine signaling through the transcription factors STAT5A and STAT5B.
272	18347089	Two members of this family, STAT5A and STAT5B (collectively called STAT5), have gained prominence in that they are activated by a wide variety of cytokines such as interleukins, erythropoietin, growth hormone, and prolactin.
273	18347089	Evidence is growing that the diverse outcomes of STAT5 signaling are not only determined by the expression of specific receptors but also by the interaction of STAT5 with cofactors and the cell-specific activity of members of the SOCS family, which negatively regulate STAT function.
274	18347089	Second, we present an example of how STAT5 can achieve cell specificity in hepatocytes through a physical and functional interaction with the glucocorticoid receptor.
275	18347089	Finally, we address an emerging issue that the interpretation of experiments from STAT5-deficient mice and cells might be compromised as these cells might reroute and reprogram cytokine signals to the "wrong" STATs and thus acquire inappropriate cues.
276	18347089	Interpretation of cytokine signaling through the transcription factors STAT5A and STAT5B.
277	18347089	Two members of this family, STAT5A and STAT5B (collectively called STAT5), have gained prominence in that they are activated by a wide variety of cytokines such as interleukins, erythropoietin, growth hormone, and prolactin.
278	18347089	Evidence is growing that the diverse outcomes of STAT5 signaling are not only determined by the expression of specific receptors but also by the interaction of STAT5 with cofactors and the cell-specific activity of members of the SOCS family, which negatively regulate STAT function.
279	18347089	Second, we present an example of how STAT5 can achieve cell specificity in hepatocytes through a physical and functional interaction with the glucocorticoid receptor.
280	18347089	Finally, we address an emerging issue that the interpretation of experiments from STAT5-deficient mice and cells might be compromised as these cells might reroute and reprogram cytokine signals to the "wrong" STATs and thus acquire inappropriate cues.
281	18460640	Growth hormone (GH) controls the physiology and pathophysiology of the liver, and its signals are conducted by two members of the family of signal transducers and activators of transcription, STAT5A and STAT5B.
282	18460640	Mice in which the Stat5a/b locus has been inactivated specifically in hepatocytes display GH resistance, the sex-specific expression of genes associated with liver metabolism and the cytochrome P-450 system is lost, and they develop hepatosteatosis.
283	18460640	Evidence is accumulating that in the absence of STAT5A/B GH aberrantly activates STAT1 and STAT3 and their downstream target genes and thereby offers a partial explanation of some of the physiological alterations observed in Stat5a/b-null mice and human patients.
284	18460640	We hypothesize that phenotypic changes observed in the absence of STAT5A/B are due to two distinct molecular consequences: first, the failure of STAT5A/B target genes to be activated by GH and second, the rerouting of GH signaling to other members of the STAT family.
285	18460640	Rerouting of GH signaling to STAT1 and STAT3 might partially compensate for the loss of STAT5A/B, but it certainly activates biological programs distinct from STAT5A/B.
286	21038417	The transcription factors signal transducer and activator of transcription 5A (STAT5A) and STAT5B negatively regulate cell proliferation through the activation of cyclin-dependent kinase inhibitor 2b (Cdkn2b) and Cdkn1a expression.
287	21239441	Because prolactin (PRL) up-regulates β-cell glucose transporter 2, glucokinase, and pyruvate dehydrogenase activities, we reasoned that glucose availability might mediate or modulate the effects of PRL on β-cell mass.
288	21239441	Here, we used male rat islets to show that PRL and glucose have differential but complementary effects on the expression of cell cyclins, cell cycle inhibitors, and various other genes known to regulate β-cell replication, including insulin receptor substrate 2, IGF-II, menin, forkhead box protein M1, tryptophan hydroxylase 1, and the PRL receptor.
289	21239441	The effects of PRL on gene expression are mirrored by β-cell overexpression of signal transducer and activator of transcription 5b and are opposed by dexamethasone.
290	21239441	An ad-small interfering RNA specific for cyclin D2 attenuates markedly the effects of PRL on islet DNA synthesis.
291	21239441	PRL up-regulates β-cell glucose uptake and utilization, whereas glucose increases islet PRL receptor expression and potentiates the effects of PRL on cell cycle gene expression and DNA synthesis.
292	21592969	Nuclear factor-kappaB (NF-kappaB) p65 interacts with Stat5b in growth plate chondrocytes and mediates the effects of growth hormone on chondrogenesis and on the expression of insulin-like growth factor-1 and bone morphogenetic protein-2.
293	21592969	Growth hormone (GH) stimulates growth plate chondrogenesis and longitudinal bone growth with its stimulatory effects primarily mediated by insulin-like growth factor-1 (IGF-1) both systemically and locally in the growth plate.
294	21592969	It has been shown that the transcription factor Stat5b mediates the GH promoting effect on IGF-1 expression and on chondrogenesis, yet it is not known whether other signaling molecules are activated by GH in growth plate chondrocytes.
295	21592969	Lastly, the inhibition of Stat5b expression in chondrocytes prevented the GH promoting effects on NF-κB-DNA binding, whereas the inhibition of NF-κB p65 expression or activity prevented the GH-dependent activation of IGF-1 and bone morphogenetic protein-2 expression.
296	21592969	Nuclear factor-kappaB (NF-kappaB) p65 interacts with Stat5b in growth plate chondrocytes and mediates the effects of growth hormone on chondrogenesis and on the expression of insulin-like growth factor-1 and bone morphogenetic protein-2.
297	21592969	Growth hormone (GH) stimulates growth plate chondrogenesis and longitudinal bone growth with its stimulatory effects primarily mediated by insulin-like growth factor-1 (IGF-1) both systemically and locally in the growth plate.
298	21592969	It has been shown that the transcription factor Stat5b mediates the GH promoting effect on IGF-1 expression and on chondrogenesis, yet it is not known whether other signaling molecules are activated by GH in growth plate chondrocytes.
299	21592969	Lastly, the inhibition of Stat5b expression in chondrocytes prevented the GH promoting effects on NF-κB-DNA binding, whereas the inhibition of NF-κB p65 expression or activity prevented the GH-dependent activation of IGF-1 and bone morphogenetic protein-2 expression.
300	21592969	Nuclear factor-kappaB (NF-kappaB) p65 interacts with Stat5b in growth plate chondrocytes and mediates the effects of growth hormone on chondrogenesis and on the expression of insulin-like growth factor-1 and bone morphogenetic protein-2.
301	21592969	Growth hormone (GH) stimulates growth plate chondrogenesis and longitudinal bone growth with its stimulatory effects primarily mediated by insulin-like growth factor-1 (IGF-1) both systemically and locally in the growth plate.
302	21592969	It has been shown that the transcription factor Stat5b mediates the GH promoting effect on IGF-1 expression and on chondrogenesis, yet it is not known whether other signaling molecules are activated by GH in growth plate chondrocytes.
303	21592969	Lastly, the inhibition of Stat5b expression in chondrocytes prevented the GH promoting effects on NF-κB-DNA binding, whereas the inhibition of NF-κB p65 expression or activity prevented the GH-dependent activation of IGF-1 and bone morphogenetic protein-2 expression.
304	22789848	Over-expression of Stat5b confers protection against diabetes in the non-obese diabetic (NOD) mice via up-regulation of CD4(+)CD25(+) regulatory T cells.
305	22789848	The total cell numbers of CD4(+) T cells and especially CD8(+) T cells in the spleen and pancreatic lymph node were increased in the Stat5b transgenic NOD mice.
306	22789848	Consistent with these findings, CD4(+) and CD8(+) T cells from the Stat5b transgenic NOD mice showed a higher proliferation capacity and up-regulation of multiple cytokines including IL-2, IFN-γ, TNF-α and IL-10 as well as anti-apoptotic gene Bcl-xl.
307	22789848	Furthermore, the number and proportion of CD4(+)CD25(+) regulatory T cells were significantly increased in transgenic mice although in vitro suppression ability of the regulatory T-cells was not affected by the transgene.
308	22789848	Our results suggest that Stat5b confers protection against diabetes in the NOD mice by regulating the numbers and function of multiple immune cell types, especially by up-regulating CD4(+)CD25(+) regulatory T cells.
309	22789848	Over-expression of Stat5b confers protection against diabetes in the non-obese diabetic (NOD) mice via up-regulation of CD4(+)CD25(+) regulatory T cells.
310	22789848	The total cell numbers of CD4(+) T cells and especially CD8(+) T cells in the spleen and pancreatic lymph node were increased in the Stat5b transgenic NOD mice.
311	22789848	Consistent with these findings, CD4(+) and CD8(+) T cells from the Stat5b transgenic NOD mice showed a higher proliferation capacity and up-regulation of multiple cytokines including IL-2, IFN-γ, TNF-α and IL-10 as well as anti-apoptotic gene Bcl-xl.
312	22789848	Furthermore, the number and proportion of CD4(+)CD25(+) regulatory T cells were significantly increased in transgenic mice although in vitro suppression ability of the regulatory T-cells was not affected by the transgene.
313	22789848	Our results suggest that Stat5b confers protection against diabetes in the NOD mice by regulating the numbers and function of multiple immune cell types, especially by up-regulating CD4(+)CD25(+) regulatory T cells.
314	22789848	Over-expression of Stat5b confers protection against diabetes in the non-obese diabetic (NOD) mice via up-regulation of CD4(+)CD25(+) regulatory T cells.
315	22789848	The total cell numbers of CD4(+) T cells and especially CD8(+) T cells in the spleen and pancreatic lymph node were increased in the Stat5b transgenic NOD mice.
316	22789848	Consistent with these findings, CD4(+) and CD8(+) T cells from the Stat5b transgenic NOD mice showed a higher proliferation capacity and up-regulation of multiple cytokines including IL-2, IFN-γ, TNF-α and IL-10 as well as anti-apoptotic gene Bcl-xl.
317	22789848	Furthermore, the number and proportion of CD4(+)CD25(+) regulatory T cells were significantly increased in transgenic mice although in vitro suppression ability of the regulatory T-cells was not affected by the transgene.
318	22789848	Our results suggest that Stat5b confers protection against diabetes in the NOD mice by regulating the numbers and function of multiple immune cell types, especially by up-regulating CD4(+)CD25(+) regulatory T cells.
319	22789848	Over-expression of Stat5b confers protection against diabetes in the non-obese diabetic (NOD) mice via up-regulation of CD4(+)CD25(+) regulatory T cells.
320	22789848	The total cell numbers of CD4(+) T cells and especially CD8(+) T cells in the spleen and pancreatic lymph node were increased in the Stat5b transgenic NOD mice.
321	22789848	Consistent with these findings, CD4(+) and CD8(+) T cells from the Stat5b transgenic NOD mice showed a higher proliferation capacity and up-regulation of multiple cytokines including IL-2, IFN-γ, TNF-α and IL-10 as well as anti-apoptotic gene Bcl-xl.
322	22789848	Furthermore, the number and proportion of CD4(+)CD25(+) regulatory T cells were significantly increased in transgenic mice although in vitro suppression ability of the regulatory T-cells was not affected by the transgene.
323	22789848	Our results suggest that Stat5b confers protection against diabetes in the NOD mice by regulating the numbers and function of multiple immune cell types, especially by up-regulating CD4(+)CD25(+) regulatory T cells.