Ignet

Gene Information

Gene symbol: ACTB

Gene name: actin, beta

HGNC ID: 132

Related Genes

#	Gene Symbol	Number of hits
1	AAVS1	1 hits
2	ACTA1	1 hits
3	ACTC1	1 hits
4	ACTN4	1 hits
5	ADIPOQ	1 hits
6	AGT	1 hits
7	AGTR1	1 hits
8	ATP2A2	1 hits
9	BDNF	1 hits
10	BRCA1	1 hits
11	CAPG	1 hits
12	CAPN10	1 hits
13	CAPN2	1 hits
14	CASP3	1 hits
15	CD44	1 hits
16	CDKN1C	1 hits
17	CHAT	1 hits
18	CLU	1 hits
19	COL1A1	1 hits
20	COL4A4	1 hits
21	COL6A1	1 hits
22	CSF1	1 hits
23	CTGF	1 hits
24	CYBA	1 hits
25	DDIT3	1 hits
26	DES	1 hits
27	DUSP1	1 hits
28	DYNC1H1	1 hits
29	EEF1A1	1 hits
30	EGF	1 hits
31	EGFR	1 hits
32	FOS	1 hits
33	GAP43	1 hits
34	GAPDH	1 hits
35	GCG	1 hits
36	GCK	1 hits
37	GFAP	1 hits
38	GHR	1 hits
39	GP2	1 hits
40	GPR180	1 hits
41	GTF3A	1 hits
42	HBA2	1 hits
43	HIST1H2BO	1 hits
44	HIST2H2BE	1 hits
45	HMOX1	1 hits
46	HRAS	1 hits
47	HSPG2	1 hits
48	IGF1	1 hits
49	IGF2	1 hits
50	IGFALS	1 hits
51	IGFBP2	1 hits
52	IL2	1 hits
53	INS	1 hits
54	INSIG1	1 hits
55	IRS1	1 hits
56	IRS4	1 hits
57	ITGA5	1 hits
58	ITGAM	1 hits
59	LASP1	1 hits
60	LCT	1 hits
61	LEP	1 hits
62	M6PR	1 hits
63	MAPK10	1 hits
64	MAPT	1 hits
65	MDK	1 hits
66	ME1	1 hits
67	MLLT3	1 hits
68	MSN	1 hits
69	MYH14	1 hits
70	MYH7	1 hits
71	NGF	1 hits
72	NOS1	1 hits
73	NPPA	1 hits
74	NPPB	1 hits
75	NRAS	1 hits
76	OPN4	1 hits
77	PCK2	1 hits
78	PCSK1N	1 hits
79	PDGFA	1 hits
80	PDGFB	1 hits
81	PDX1	1 hits
82	PHB	1 hits
83	PPP1R3C	1 hits
84	PTPRC	1 hits
85	REN	1 hits
86	RHOD	1 hits
87	RNASEN	1 hits
88	RPE65	1 hits
89	RPS27A	1 hits
90	RS1	1 hits
91	SERPINE1	1 hits
92	SLC2A2	1 hits
93	SLC37A4	1 hits
94	SLC9A1	1 hits
95	SLC9A3R2	1 hits
96	SMARCA1	1 hits
97	SST	1 hits
98	STAT3	1 hits
99	TG	1 hits
100	TGFA	1 hits
101	TGFB1	1 hits
102	TMOD3	1 hits
103	TP63	1 hits
104	TPO	1 hits
105	TSHR	1 hits
106	TUBA1A	1 hits
107	TUBB2A	1 hits
108	TUBB3	1 hits
109	TUBB4	1 hits
110	VCL	1 hits
111	VEGFA	1 hits
112	VWF	1 hits

Related Sentences

#	PMID	Sentence
1	1381373	A variety of hormones and growth factors that regulate the growth and function of these thyroid cells were found to decrease class I RNA levels: serum, insulin or insulin-like growth factor-I (IGF-I), and hydrocortisone.
2	1381373	The class I response to TSH, serum, insulin, IGF-I, or hydrocortisone is specific, in that the same agents do not similarly affect TSH receptor, thyroglobulin, thyroid peroxidase, malic enzyme, or beta-actin RNA levels.
3	1513101	Effects of diabetes and insulin on expression of kallikrein and renin genes in the kidney.
4	1513101	To investigate the molecular mechanisms underlying these changes, we examined the effects of diabetes and insulin treatment on renal kallikrein and renal renin mRNA levels and the activities of these enzymes.
5	1513101	This was associated with reduced plasma renin concentration (4.5 +/- 0.2 vs. 10.5 +/- 1.6 ng Ang I/ml/hr, D vs.
6	1513101	However, renal renin concentration was unchanged (0.84 +/- 0.17 vs. 0.84 +/- 1.3 micrograms Ang I/mg protein/hr, D vs.
7	1513101	However, renal renin concentration was increased (1.49 +/- 0.27 micrograms Ang I/mg protein/hr) compared to C rats (P less than 0.05). beta-actin mRNA levels were unchanged in either diabetic rat group.
8	1707859	Hybridization of poly(A)+ RNA northern blots revealed only the cytoskeletal beta-actin message; by using the more sensitive solution hybridization assay, the plasminogen activator-inhibitor 1 (PAI-1) and von Willebrand factor (vWF) mRNAs were quantified.
9	1707859	The prevalence of these transcripts in the retinal microvessels was 0.04 x 10(6) copies/ng RNA for PAI-1 and 0.14 x 10(6) copies/ng RNA for vWF, much less than the prevalence in human umbilical vein endothelial cells (1.93 x 10(6) and 3.90 x 10(6), respectively).
10	2004618	Orchiectomy resulted in 39% and 41% reductions in the levels of EGFR mRNA and EGF binding, respectively, within 2 weeks.
11	2004618	The hepatic levels of EGFR mRNA and EGF binding in females were 37% and 36% of those in males, respectively, and were not affected by ovariectomy, whereas treatment of females with TP (100 micrograms/mouse.day) increased EGFR to normal male levels within 1 week.
12	2004618	On the other hand, neither orchiectomy nor androgen treatment affected levels of mRNAs for EGFR in the kidney or mRNAs for the structural protein beta-actin in the liver.
13	2004618	To examine whether testosterone directly increased EGFR levels in the liver, TP (1.0 mg) pellets were implanted into the spleen of orchiectomized mice, so that testosterone released from the pellets reached the liver through the portal vein but did not enter the systemic circulation due to rapid clearance by the liver.
14	2004618	The heptic levels of EGFR mRNA and EGF binding in orchiectomized mice were restored to normal male levels by intrasplenic implantation of TP (1.0 mg) pellets.
15	2004618	This treatment also increased the hepatic levels of EGFR mRNA and EGF binding in female mice by 61% and 68%, respectively.
16	2004618	In addition, sialoadenectomy, which reduced plasma EGF, as well as EGF antiserum treatment did not affect the androgen-dependent increase in EGFR levels in the liver, suggesting that endogenous EGF is not involved in the androgenic regulation of hepatic EGFR levels.
17	2164948	The levels of mRNAs encoding the alpha 1 chain of collagen IV and the B1 chain of laminin were assayed in the lenses and retinas of long-term (28-week) diabetic and galactosaemic rats in order to gain some insight into the effects on basement membrane (BM) synthesis in these tissues. mRNAs coding for beta-actin, glucose transporter protein and the alpha 2 catalytic subunit of Na+,K(+)-ATPase were also assayed to determine whether any effects on BM-coding mRNA levels were specific.
18	2164948	In the same samples, the level of the glucose transporter protein mRNA was found to be elevated significantly in the diabetic tissue, whereas the mRNAsen coding beta-actin and alpha 2 Na+,K(+)-ATPase were unaffected in comparison with age-matched controls.
19	2164948	The levels of mRNAs encoding the alpha 1 chain of collagen IV and the B1 chain of laminin were assayed in the lenses and retinas of long-term (28-week) diabetic and galactosaemic rats in order to gain some insight into the effects on basement membrane (BM) synthesis in these tissues. mRNAs coding for beta-actin, glucose transporter protein and the alpha 2 catalytic subunit of Na+,K(+)-ATPase were also assayed to determine whether any effects on BM-coding mRNA levels were specific.
20	2164948	In the same samples, the level of the glucose transporter protein mRNA was found to be elevated significantly in the diabetic tissue, whereas the mRNAsen coding beta-actin and alpha 2 Na+,K(+)-ATPase were unaffected in comparison with age-matched controls.
21	2477846	Furthermore, levels of submandibular prepro-EGF mRNA in these diabetic mice were decreased almost in parallel with the glandular EGF concentrations, while there was no change in the levels of submandibular beta-actin mRNA and kidney prepro-EGF mRNA.
22	2477846	Insulin administration to streptozotocin-treated mice almost completely reversed the decrease in EGF content in the submandibular gland, substantially elevated the level of the glandular prepro-EGF mRNA and plasma EGF concentration, and increased the size of the granular convoluted tubules in the gland.
23	2477846	These results indicate that EGF deficiency occurs in diabetes mellitus and that insulin may be important in maintaining the normal level of EGF in the submandibular gland and plasma.
24	2664474	The addition of TSH to FRTL-5 thyroid cells induces a 7- to 8-fold increase in the steady state level of malic enzyme [L-malate-NADP+ oxidoreductase (decarboxylating); EC 1.1.1.40] mRNA, but does not alter beta-actin mRNA levels.
25	2664474	Insulin alone or together with TSH has no effect on malic enzyme mRNA.
26	7485483	These include altered expression of insulin-regulated genes such as glucose-6-phosphatase (G-6-Pase), phosphoenolpyruvate carboxykinase (PEPCK), and beta-actin, and genes such as CL-6 and map kinase phosphatase-1 (MKP-1) that were previously unlinked to insulin action in animals.
27	7485483	Abnormal elevation of mRNAs encoding G-6-Pase, MKP-1, and PEPCK in the time 0 diabetic liver results in decreased induction after partial hepatectomy.
28	7485483	Other genes, such as CL-6 and beta-actin, are induced at a lower level in the hepatectomized diabetic animals.
29	7485483	These include altered expression of insulin-regulated genes such as glucose-6-phosphatase (G-6-Pase), phosphoenolpyruvate carboxykinase (PEPCK), and beta-actin, and genes such as CL-6 and map kinase phosphatase-1 (MKP-1) that were previously unlinked to insulin action in animals.
30	7485483	Abnormal elevation of mRNAs encoding G-6-Pase, MKP-1, and PEPCK in the time 0 diabetic liver results in decreased induction after partial hepatectomy.
31	7485483	Other genes, such as CL-6 and beta-actin, are induced at a lower level in the hepatectomized diabetic animals.
32	7538809	The levels of mRNA coding for transforming growth factor-beta 1, tenascin, and laminin B1 increased 1.9-, 2.0-, and 1.7-fold, respectively, whereas platelet-derived growth factor (PDGF)-B, alpha 1(IV) collagen, 72-kd collagenase, alpha-smooth muscle actin, and beta-actin mRNA remained stable in the diabetic mice.
33	7538809	There was no increase in cell number per glomerulus after the onset of diabetes, a finding consistent with stable PDGF-B and alpha-smooth muscle actin mRNA levels.
34	7538809	These findings provide evidence that increased glomerular transforming growth factor-beta 1, but not PDGF-B, mRNA is associated with the up-regulation of tenascin and laminin expression after advanced glycosylation endproduct accumulation, early after the onset of diabetes.
35	7685720	In contrast, glucose infusion resulted in a twofold increase in insulin mRNA levels and did not significantly alter levels of beta-actin mRNA.
36	7693843	Expression of the adipocyte fatty acid-binding protein in streptozotocin-diabetes: effects of insulin deficiency and supplementation.
37	7693843	The adipocyte fatty acid-binding protein, aP2 or ALBP, is an abundant cytosolic protein postulated to function in binding and intracellular transport of long-chain fatty acids.
38	7693843	An average 75% decrease in mRNA for aP2 (relative to mRNA for beta-actin) was observed in all diabetic rats at 7 days post-STZ injection.
39	7693843	Insulin supplementation rapidly (2 h) restored aP2 mRNA and the insulin effect was cycloheximide-sensitive.
40	7693843	Nuclear transcription assays measured a 60% decrease in transcription of the aP2 gene in diabetic rats that was reversed by insulin administration.
41	7693843	Decreases in aP2 protein were rapidly reversed by insulin administration.
42	7693843	The decrease in aP2 mRNA was delayed in onset when compared with the rapid decline (at day 2 of diabetes) of mRNA for the lipogenic enzyme, fatty acid synthase, and with the accelerated depletion of adipose tissue lipid.
43	7700017	Diabetes mellitus is characterized by alterations in the intrarenal renin-angiotensin system, including decreases in glomerular angiotensin II (Ang II) receptor density.
44	7700017	Concomitant insulin treatment reversed the decrease in specific binding of 125I Ang II to basolateral membranes (109 +/- 26% of control; N = 3) and to brush border membranes (85 +/- 17% of control; N = 6).
45	7700017	In order to determine if changes in expression of type-1 Ang II receptors (AT1R) accompanied the changes in binding, quantitative polymerase chain reaction of AT1R mRNA was performed and expressed as the ratio of the amplified AT1R to that of an Msc1/Msc1 internal deletion mutant and normalized to that of beta-actin.
46	7700017	In total RNA from proximal tubule suspensions of diabetic animals, AT1R mRNA expression decreased by 38% (21 +/- 3 vs. 13 +/- 2 cpm AT1R/cpm deletion mutant/cpm beta actin/10(6); N = 4; P < 0.0025).
47	7700017	Insulin treatment reverted AT1R mRNA expression to control levels (22 +/- 3 cpm AT1R/cpm deletion mutant/cpm beta actin/10(6); P < 0.001 compared to the untreated group).
48	7700017	Diabetes mellitus is characterized by alterations in the intrarenal renin-angiotensin system, including decreases in glomerular angiotensin II (Ang II) receptor density.
49	7700017	Concomitant insulin treatment reversed the decrease in specific binding of 125I Ang II to basolateral membranes (109 +/- 26% of control; N = 3) and to brush border membranes (85 +/- 17% of control; N = 6).
50	7700017	In order to determine if changes in expression of type-1 Ang II receptors (AT1R) accompanied the changes in binding, quantitative polymerase chain reaction of AT1R mRNA was performed and expressed as the ratio of the amplified AT1R to that of an Msc1/Msc1 internal deletion mutant and normalized to that of beta-actin.
51	7700017	In total RNA from proximal tubule suspensions of diabetic animals, AT1R mRNA expression decreased by 38% (21 +/- 3 vs. 13 +/- 2 cpm AT1R/cpm deletion mutant/cpm beta actin/10(6); N = 4; P < 0.0025).
52	7700017	Insulin treatment reverted AT1R mRNA expression to control levels (22 +/- 3 cpm AT1R/cpm deletion mutant/cpm beta actin/10(6); P < 0.001 compared to the untreated group).
53	7700017	Diabetes mellitus is characterized by alterations in the intrarenal renin-angiotensin system, including decreases in glomerular angiotensin II (Ang II) receptor density.
54	7700017	Concomitant insulin treatment reversed the decrease in specific binding of 125I Ang II to basolateral membranes (109 +/- 26% of control; N = 3) and to brush border membranes (85 +/- 17% of control; N = 6).
55	7700017	In order to determine if changes in expression of type-1 Ang II receptors (AT1R) accompanied the changes in binding, quantitative polymerase chain reaction of AT1R mRNA was performed and expressed as the ratio of the amplified AT1R to that of an Msc1/Msc1 internal deletion mutant and normalized to that of beta-actin.
56	7700017	In total RNA from proximal tubule suspensions of diabetic animals, AT1R mRNA expression decreased by 38% (21 +/- 3 vs. 13 +/- 2 cpm AT1R/cpm deletion mutant/cpm beta actin/10(6); N = 4; P < 0.0025).
57	7700017	Insulin treatment reverted AT1R mRNA expression to control levels (22 +/- 3 cpm AT1R/cpm deletion mutant/cpm beta actin/10(6); P < 0.001 compared to the untreated group).
58	7861156	Following 12 weeks of diabetes, BDNF mRNA levels were increased approximately two- to threefold in L4 and L5 dorsal root ganglia (DRG), and in sciatic nerve, NGF mRNA levels were raised 1.65-fold.
59	7861156	Intensive insulin treatment of diabetic rats for the final 4 weeks of the 12-week period of diabetes reversed the up-regulation of BDNF mRNA in DRG and muscle and NGF mRNA in sciatic nerve.
60	7861156	All diabetes-induced changes in neurotrophin mRNA were not paralleled by similar alterations in the levels of beta-actin mRNA in muscle and nerve, or of GAP-43 mRNA in DRG and nerve.
61	7967355	RNA samples were reverse transcribed (RT) and subjected to polymerase chain reaction (PCR) amplication with specific 5' and 3' primers for rat transforming growth factor (TGF-beta 1) and beta-actin.
62	7967355	RT-PCR analysis revealed that glomerular TGF-beta 1 mRNA levels increased relative to beta-actin as early as 24 hours after the onset of hyperglycemia, reaching a plateau after 96 hours that was sustained at one and two weeks.
63	7967355	Intensive insulin treatment to normalize blood glucose levels attenuated the rise in glomerular and renal cortical TGF-beta 1 mRNA.
64	7967355	Normalization of blood glucose levels with insulin treatment attenuates the increase in TGF-beta 1 expression.
65	7967355	RNA samples were reverse transcribed (RT) and subjected to polymerase chain reaction (PCR) amplication with specific 5' and 3' primers for rat transforming growth factor (TGF-beta 1) and beta-actin.
66	7967355	RT-PCR analysis revealed that glomerular TGF-beta 1 mRNA levels increased relative to beta-actin as early as 24 hours after the onset of hyperglycemia, reaching a plateau after 96 hours that was sustained at one and two weeks.
67	7967355	Intensive insulin treatment to normalize blood glucose levels attenuated the rise in glomerular and renal cortical TGF-beta 1 mRNA.
68	7967355	Normalization of blood glucose levels with insulin treatment attenuates the increase in TGF-beta 1 expression.
69	8011322	Expression of insulin-like growth factors I and II in conceptuses from normal and diabetic mice.
70	8011322	Insulin-like growth factors (IGF-I and IGF-II) play an important regulatory role in fetal growth and development.
71	8011322	In situ hybridization histochemistry was employed to investigate the distribution and abundance of IGF-I and IGF-II in peri-implantation and postimplantation conceptuses from normal and streptozotocin-treated diabetic mice.
72	8011322	The entire uterine horn was prepared for hybridization with antisense and sense alpha 35S-dATP labeled oligonucleotide probes for IGF-I, IGF-II, and mouse beta-actin.
73	8171758	Utilizing cDNA probes, the gene products sulfated glycoprotein-2 (SGP-2), transforming growth factor-beta (TGF-beta), beta-actin (beta-actin), N-ras and beta nerve growth factor (beta-NGF), were quantitated in bladders of male Sprague-Dawley rats at 1, 2, 4 and 6 weeks after induction of diabetes with streptozotocin (STZ). beta-actin and SGP-2 expression were transiently increased at 1 and 4 weeks after induction, respectively.
74	8171758	N-ras was reduced at all times compared with control rat bladders.
75	8781771	To examine the course of biosynthetic changes relevant to the process, retinal expression of collagen IV and fibronectin were compared in rats fed a 30% galactose diet or a control diet for 5 or 9 weeks.
76	8781771	The levels of alpha 1 (IV) collagen and fibronectin mRNAs were measured relative to an internal standard (beta-actin mRNA).
77	8781771	The proportion of EIIIA+ to EIIIA- fibronectin transcripts was similar in the retinas of control and galactose-fed rats, which, however, showed increased levels of both fibronectin and collagen IV mRNAs in the presence of unchanged beta-actin mRNA levels.
78	8781771	An upward trend was detected by 5 weeks of galactose feeding; and after 9 weeks the fibronectin/actin ratio was 1.2 +/- 0.3 vs 0.8 +/- 0.2 in controls (p = 0.015) and the collagen IV/actin ratio was 1.3 +/- 0.3 vs 0.9 +/- 0.2 in controls (p = 0.04).
79	8781771	To examine the course of biosynthetic changes relevant to the process, retinal expression of collagen IV and fibronectin were compared in rats fed a 30% galactose diet or a control diet for 5 or 9 weeks.
80	8781771	The levels of alpha 1 (IV) collagen and fibronectin mRNAs were measured relative to an internal standard (beta-actin mRNA).
81	8781771	The proportion of EIIIA+ to EIIIA- fibronectin transcripts was similar in the retinas of control and galactose-fed rats, which, however, showed increased levels of both fibronectin and collagen IV mRNAs in the presence of unchanged beta-actin mRNA levels.
82	8781771	An upward trend was detected by 5 weeks of galactose feeding; and after 9 weeks the fibronectin/actin ratio was 1.2 +/- 0.3 vs 0.8 +/- 0.2 in controls (p = 0.015) and the collagen IV/actin ratio was 1.3 +/- 0.3 vs 0.9 +/- 0.2 in controls (p = 0.04).
83	8781982	Streptozotocin induction of diabetes in rats leads to increased insulin-like growth factor-II/mannose-6-phosphate receptor mRNA expression in kidney but not in lung or heart.
84	8781982	We have measured the expression of IGF-II/M6P receptor mRNA in rat kidney, lung and heart after streptozotocin induction of diabetes.
85	8781982	In solution hybridization/RNAse protection experiments, specific IGF-II/M6P receptor and beta-actin transcripts were detected in the RNA samples from all tissues examined.
86	8781982	To gain additional evidence for the expression of IGF-II/M6P receptor RNA in the tissues examined, Northern blotting experiments were performed: a major 9 kb RNA species was detected on the blots.
87	8781982	Interestingly, streptozotocin-induced onset of diabetes led to a significant increase in the expression of IGF-II/M6P receptor mRNA in the kidney but not in lung and heart whereas no change in actin mRNA expression was measured.
88	8781982	Insulin treatment did not prevent the increase of IGF-II/M6P receptor mRNA expression during short-term treatment (1-9 days).
89	8808981	Samples were subjected to slot-blot analysis by using homologous probes for insulin, glucagon, somatostatin, glucose transporter-2 (glut-2), glucokinase, elastase-I, and beta-actin.
90	8808981	This paralleled decreases in glut-2 (p = .001) mRNA levels, but it was in contrast with glucokinase mRNA levels which increased markedly (p = .0003).
91	8808981	Somatostatin mRNA levels were unchanged, glucagon mRNA levels decreased modesty (p = .01), and mRNA levels for elastase-I and beta-actin increased with age (p = .0001 for either one).
92	8808981	Samples were subjected to slot-blot analysis by using homologous probes for insulin, glucagon, somatostatin, glucose transporter-2 (glut-2), glucokinase, elastase-I, and beta-actin.
93	8808981	This paralleled decreases in glut-2 (p = .001) mRNA levels, but it was in contrast with glucokinase mRNA levels which increased markedly (p = .0003).
94	8808981	Somatostatin mRNA levels were unchanged, glucagon mRNA levels decreased modesty (p = .01), and mRNA levels for elastase-I and beta-actin increased with age (p = .0001 for either one).
95	9011569	The results of reporter gene analyses revealed that the insulin gene promoter is more sensitive to glycation than the control beta-actin gene promoter; approximately 50 and 80% of the insulin gene promoter activity was lost when the cells were kept for 3 d in the presence of 40 and 60 mM D-ribose, respectively.
96	9011569	Also, gel mobility shift analyses using specific antiserum revealed decrease in the DNA-binding activity of an insulin gene transcription factor, PDX-1/IPF1/STF-1.
97	9032395	The Rep proteins of adeno-associated virus type 2 (AAV) are known to bind to Rep recognition sequences (RRSs) in the AAV inverted terminal repeats (ITRs), the AAV p5 promoter, and the preferred AAV integration site in human chromosome 19, called AAVS1.
98	9032395	We used the 16-mer core sequences of the RRSs in the AAV ITRs and AAVS1 separately as query sequences and identified 18 new RRSs in or flanking the genes coding for the following: tyrosine kinase activator protein 1 (TKA-1); colony stimulating factor-1; insulin-like growth factor binding protein 2 (IGFBP-2); histone H2B.1; basement membrane heparan sulfate proteoglycan, also known as perlecan; the AF-9 gene product, which is involved in the chromosomal translocation t (9:11)(p22:q23); the betaB subunit of the hormone known as inhibin; interleukin-2 enhancer binding factor; an endoplasmic reticulum-Golgi intermediate compartment resident protein called p63; a global transcription activator (hSNF2L); the beta-actin repair domain; a retinoic acid-inducible factor, also known as midkine; a breast tumor autoantigen; a growth-arrest- and DNA-damage-inducible protein called gadd45; the cyclin-dependent kinase inhibitor called KIP2, which inhibits several G1 cyclin-cyclin-dependent kinase complexes; and the hereditary breast and ovarian cancer gene (BRCA1).
99	9325287	Leptin normalizes the impaired response of proinsulin mRNA to long chain fatty acids in heterozygous Zucker diabetic fatty rats.
100	9325287	To determine if underleptinization of islets of Zucker diabetic fatty (ZDF) rats is the proximal cause of their inability to compensate for obesity, we compared the proinsulin/beta-actin mRNA ratio in heterozygous (fa/+) ZDF rats with that of wild-type (+/+) and homozygous (fa/fa) ZDF rats.
101	9325287	The presence of leptin (20 ng/ml) in the culture medium increased the FFA-induced response of proinsulin mRNA of fa/+ islets to that of +/+ islets while reducing FFA incorporation into triglycerides.
102	9325287	The leptin-induced improvement in the proinsulin mRNA response was independent of any changes in glucose usage.
103	9330585	Ob mRNA/beta-actin concentration in fat biopsies from abdominal subcutaneous adipose tissue was unchanged after 6 days of fasting (1.50 +/- 0.40 vs 1.47 +/- 0.36 arbitrary units, not significant), whereas serum leptin levels decreased significantly from 53.8 +/- 4.7 to 30.7 +/- 2.0 ng/ml (P < 0.0001) during the same period.
104	9330585	No significant correlations were found between insulin-stimulated glucose uptake and serum leptin concentration, either prior to the fast or after the fast.
105	9330585	Furthermore, after 6 days of fasting insulin was able to increase the serum level of leptin significantly, indicating that the effect of insulin on the level of leptin is dependent on the nutritional state.
106	9421374	Ex vivo, a gradual decrement of both GLUT2 protein and mRNA expression was found in pancreatic islets isolated from MLD-STZ-treated C57BL/6 male mice, whereas mRNA expression of beta-actin, glucokinase, and proinsulin remained unaffected.
107	9421374	The STZ-induced reduction of GLUT2 protein and mRNA was not due to an essential loss of beta-cells, because ex vivo, not only the total RNA yield and protein content in isolated islets, but also proinsulin mRNA expression, failed to differ significantly in the differently treated groups.
108	9730011	Compared with control animals without MI, the atrial ANP/beta-actin mRNA ratio in rats with MI was increased to 195% in diabetic animals and 213% in nondiabetic animals.
109	9730011	In the left ventricle, however, the ANP/beta-actin mRNA ratio in diabetic animals with MI was increased to only 131% compared with control animals, whereas the corresponding increase in nondiabetic animals was 240% (p<0.05).
110	9730011	Compared with control animals without MI, the atrial ANP/beta-actin mRNA ratio in rats with MI was increased to 195% in diabetic animals and 213% in nondiabetic animals.
111	9730011	In the left ventricle, however, the ANP/beta-actin mRNA ratio in diabetic animals with MI was increased to only 131% compared with control animals, whereas the corresponding increase in nondiabetic animals was 240% (p<0.05).
112	9745713	We used transmission electron microscopy to study the fine structure of STZ-diabetic and non-diabetic SMC in primary culture and immunological methods for the determination of the proportions of alpha-smooth muscle actin (alpha-SM) and nonmuscle beta-actin (beta-NM) isoforms.
113	10079029	The BNP mRNA/beta-actin mRNA ratio in right ventricle of nondiabetic rats with MI was increased to 350+/-60%, however, in diabetic rats with MI, that was slightly increased to 200+/-50% (P < 0.01).
114	10079029	Cardiac BNP synthesis in diabetic rats completely reverted to control levels after insulin therapy.
115	10871206	We have previously shown that mRNA levels for ET-1, ET-3, and their receptors are upregulated under hyperhexosemic conditions.
116	10871206	Semiquantitative reverse transcription-polymerase chain reaction for fibronectin and collagen alpha1 (IV) was conducted after 1 month of follow-up with comparison to beta-actin housekeeping gene using slot blot hybridization and densitometry.
117	11015588	We demonstrated that plasma leptin levels are approximately twofold higher in aP212 transgenic mice compared with their respective controls, whereas ubiquitous expression of agouti (under the control of beta-actin promoter, BAP20) led to a sixfold increase in leptin.
118	11015588	Insulin treatment of aP212 mice increased adipocyte leptin content without affecting plasma leptin levels.
119	11015588	Agouti but not insulin significantly increased leptin secretion, indicating that insulin enhances leptin synthesis but not secretion while Agouti increases both leptin synthesis and secretion.
120	11158048	Gene expression of GHR and GHRtr in adipose tissue and skeletal muscle was determined and expressed relative to the expression of beta-actin.
121	11283524	The number of alpha-globin genes present in the subjects was determined by the intensity of alpha1 and alpha2 bands normalized with that of beta-actin when using densitometry.
122	11489416	Female mosquitoes of the species Aedes aegypti were fed with HGV-infected human blood and assayed 1, 24, 48, 72 and 96 h after the blood meal for viral RNA, human glyceraldehyde-3-phosphate dehydrogenase mRNA, human beta-actin DNA and A. aegypti actin mRNA by total nucleic acid extraction, reverse transcription and PCR.
123	11804845	Western analysis indicated that SGLT1 and GLUT5 protein levels were also 4.3- and 4.1-fold higher in diabetic patients.
124	11804845	This was associated with threefold increases in SGLT1 and GLUT5 mRNA measured by Northern blotting.
125	11804845	Analysis of other BBM proteins indicated that the activity and abundance of sucrase and lactase were increased by 1.5- to 2-fold and the level of the structural proteins villin and beta-actin was enhanced 2-fold in diabetic patients compared with controls.
126	11804845	The increase in the capacity of the intestine to absorb monosaccharides in human NIDDM is due to a combination of intestinal structural change with a specific increase in the expression of the monosaccharide transporters SGLT1, GLUT5, and GLUT2.
127	11890964	In this experiment we examined the effects of peripheral and central leptin administration in male and female beta-actin promoter (BAPa) mice that express agouti protein ectopically and have a phenotype that includes obesity and diabetes which is exaggerated in males compared with females.
128	12137914	In this study, we report that the glucose transporter 2 (GLUT2) and glucokinase (GK) are target molecules for ALX.
129	12137914	The mRNA expression of beta-actin was also slightly affected with time after ALX exposure, the proinsulin mRNA, however, remained unaffected as well as the pancreatic total insulin content.
130	12137914	Injections of multiple low doses (MLD) of STZ reduced GLUT2 expression only, but failed to affect expression of GK and proinsulin as well as beta-actin as internal control.
131	12137914	In this study, we report that the glucose transporter 2 (GLUT2) and glucokinase (GK) are target molecules for ALX.
132	12137914	The mRNA expression of beta-actin was also slightly affected with time after ALX exposure, the proinsulin mRNA, however, remained unaffected as well as the pancreatic total insulin content.
133	12137914	Injections of multiple low doses (MLD) of STZ reduced GLUT2 expression only, but failed to affect expression of GK and proinsulin as well as beta-actin as internal control.
134	12206992	To evaluate the impact of SERCA2a overexpression on SR Ca2+ handling in diabetic CM, we 1) generated transgenic rats harboring a human cytomegalovirus enhancer/chicken beta-actin promotor-controlled rat SERCA2 transgene (SERCA2-TGR), 2) characterized their SR phenotype, and 3) examined whether transgene expression may rescue SR Ca2+ transport in streptozotocin-induced diabetes.
135	12624601	The phlorizin-treated diabetic rats showed a significant decrease in the ratio of nNOS to beta-actin mRNA compared with diabetic rats.
136	12679469	Monocyte NADPH oxidase subunit p22(phox) and inducible hemeoxygenase-1 gene expressions are increased in type II diabetic patients: relationship with oxidative stress.
137	12679469	We determined whether in type 2 diabetes mononuclear cells, NADPH oxidase and the inducible hemeoxygenase (HO-1) gene expressions are activated.
138	12679469	In monocytes from 25 outpatients with type 2 diabetes, p22(phox) gene expression was higher (0.71 +/- 0.09 p22(phox)/beta-actin gene expression ratio) than that observed in 19 controls (0.56 +/- 0.09, P < 0.001).
139	12679469	Similarly, HO-1 gene expression was significantly higher in diabetic patients (0.77 +/- 0.12 HO-1/beta-actin gene expression ratio) than in controls (0.41 +/- 0.14, P < 0.001).
140	12679469	The p22(phox) and HO-1 gene expressions were also determined during (plasma glucose 363 +/- 40 mg/dl) and after (125 +/- 11 mg/dl) metabolic decompensation in 10 type 2 diabetic patients.
141	12679469	The correction of the metabolic milieu was associated with a 19% +/- 3% (P < 0.01) and 30% +/- 3% (P < 0.01) decrease in the p22(phox) and HO-1 gene expressions, respectively.
142	12679469	Decompensated type 2 diabetes is associated with increased p22(phox) and HO-1 gene expressions in circulating monocytes; the metabolic normalization reduces but does not normalize this activation.
143	12679469	Monocyte NADPH oxidase subunit p22(phox) and inducible hemeoxygenase-1 gene expressions are increased in type II diabetic patients: relationship with oxidative stress.
144	12679469	We determined whether in type 2 diabetes mononuclear cells, NADPH oxidase and the inducible hemeoxygenase (HO-1) gene expressions are activated.
145	12679469	In monocytes from 25 outpatients with type 2 diabetes, p22(phox) gene expression was higher (0.71 +/- 0.09 p22(phox)/beta-actin gene expression ratio) than that observed in 19 controls (0.56 +/- 0.09, P < 0.001).
146	12679469	Similarly, HO-1 gene expression was significantly higher in diabetic patients (0.77 +/- 0.12 HO-1/beta-actin gene expression ratio) than in controls (0.41 +/- 0.14, P < 0.001).
147	12679469	The p22(phox) and HO-1 gene expressions were also determined during (plasma glucose 363 +/- 40 mg/dl) and after (125 +/- 11 mg/dl) metabolic decompensation in 10 type 2 diabetic patients.
148	12679469	The correction of the metabolic milieu was associated with a 19% +/- 3% (P < 0.01) and 30% +/- 3% (P < 0.01) decrease in the p22(phox) and HO-1 gene expressions, respectively.
149	12679469	Decompensated type 2 diabetes is associated with increased p22(phox) and HO-1 gene expressions in circulating monocytes; the metabolic normalization reduces but does not normalize this activation.
150	12682826	To address these issues, a C-terminus regulatory domain of NHE-1 was cloned and sequenced from normal human placentas, and was used to prepare a GST-fusion protein for raising polyclonal antibodies.
151	12682826	The level of NHE-1 protein was decreased significantly ( p<0.05) in diabetic placentas, whereas beta-actin, an internal control, remained unaltered.
152	12682826	Interestingly, the levels of NHE-1 mRNA and beta-actin mRNA did not change in diabetic pregnancies.
153	12682826	To address these issues, a C-terminus regulatory domain of NHE-1 was cloned and sequenced from normal human placentas, and was used to prepare a GST-fusion protein for raising polyclonal antibodies.
154	12682826	The level of NHE-1 protein was decreased significantly ( p<0.05) in diabetic placentas, whereas beta-actin, an internal control, remained unaltered.
155	12682826	Interestingly, the levels of NHE-1 mRNA and beta-actin mRNA did not change in diabetic pregnancies.
156	12727110	The expression of the GLP-1 gene was driven by a chicken beta-actin promoter (pbetaGLP1).
157	12727110	Coculture assay of the GLP-1 plasmid-transfected cells with isolated rat islet cells demonstrated that GLP-1 increased insulin secretion by twofold, compared to controls during a hyperglycemic challenge.
158	14649687	Immunohistochemical staining for anticollagen type IV, integrin alpha5, laminin, smooth muscle beta-actin, procollagen type I, and desmin was evaluated.
159	14758569	Here, we describe differential in vitro effects of STZ and ALX on beta-cell molecules that are essential for glucose transport and metabolism, the glucose transporter 2 (GLUT2) and glucokinase (GK), respectively.
160	14758569	Both STZ and ALX failed to affect the mRNA expression of proinsulin and of beta-actin.
161	15012590	ProSAAS is a neuroendocrine peptide precursor that potently inhibits prohormone convertase 1 in vitro.
162	15012590	To explore the function of proSAAS and its derived peptides, transgenic mice were created which express proSAAS using the beta-actin promoter.
163	15012590	In the pituitary, the levels of several fully processed peptides in transgenic mice were not reduced compared with wild-type mice, indicating that the proSAAS transgene did not affect prohormone convertase 1 activity in this tissue.
164	15012590	Because the inhibitory potency of proSAAS-derived peptides towards prohormone convertase 1 is much greater in the absence of carboxypeptidase E activity, the proSAAS transgene was also expressed in carboxypeptidase E-deficient Cpe (fat/fat) mice.
165	15012590	Although the transgenic mice were born in the expected frequency, 21 of 22 proSAAS transgenic Cpe (fat/fat) mice died between 11 and 26 weeks of age, presumably due to greatly elevated blood glucose.
166	15012590	The levels of several pituitary peptides were significantly reduced in the proSAAS transgenic Cpe (fat/fat) mice relative to non-transgenic Cpe (fat/fat) mice, suggesting that the transgene inhibited prohormone convertase 1 in these mice.
167	15012590	Taken together, these results are consistent with a role for proSAAS-derived peptides as neuropeptides that influence body weight independently of their function as inhibitors of prohormone convertase 1.
168	15251955	Beta-actin mRNA was also assayed and results are expressed as a ratio of RHO to beta-actin mRNA.
169	15562250	We determined body composition, abdominal fat distribution, plasma lipids, and abdominal subcutaneous fat gene expression of leptin, TNF-alpha, IL-6, PAI-1, and adiponectin in 20 obese, middle-aged women (BMI, 32.7 +/- 0.8 kg/m2; age, 57 +/- 1 yr).
170	15562250	In all women, visceral fat volume was negatively related to leptin (r = -0.46, P < 0.05) and tended to be negatively related to adiponectin (r = -0.38, P = 0.09) gene expression.
171	15562250	Among the nondiabetic women, fasting insulin (r = 0.69, P < 0.01), 2-h insulin (r = 0.56, P < 0.05), and HOMA index (r = 0.59, P < 0.05) correlated positively with TNF-alpha gene expression; fasting insulin (r = 0.54, P < 0.05) was positively related to, and 2-h insulin (r = 0.49, P = 0.06) tended to be positively related to, IL-6 gene expression; and glucose area (r = -0.56, P < 0.05) was negatively related to, and insulin area (r = -0.49, P = 0.06) tended to be negatively related to, adiponectin gene expression.
172	15562250	Also, adiponectin gene expression was significantly lower in women with vs. without the metabolic syndrome (adiponectin-beta-actin ratio, 2.26 +/- 0.46 vs. 3.31 +/- 0.33, P < 0.05).
173	15692059	The present study examined the influence of streptozotocin-induced diabetes on the renal expression of bradykinin (BK) B2 receptors (B2KR), connective tissue growth factor (CTGF), transforming growth factor-beta (TGF-beta), and TGF-beta type II receptor (TGF-betaRII) and assessed the signaling mechanisms through which B2KR activation may promote glomerular injury.
174	15692059	Eight weeks after the induction of diabetes, renal mRNA levels of B2KR, CTGF, and TGF-beta as well as protein levels of CTGF and TGF-betaRII were measured in control (C), diabetic (D), and insulin-treated diabetic (D+I) rats.
175	15692059	Renal B2KR and TGF-beta mRNA levels expressed relative to beta-actin mRNA levels and CTGF and TGF-betaRII protein levels were significantly increased in D and D+I rats compared with C rats (P < 0.03, n = 5).
176	15692059	To assess the contribution of B2KR activation on modulating the expression of CTGF, TGF-betaRII, and collagen I, mesangial cells (MC) were treated with BK (10(-8) M) for 24 h and CTGF and TGF-betaRII protein levels were measured by Western blots and collagen I mRNA levels were measured by RT-PCR.
177	15692059	In addition, a marked increase in collagen I mRNA levels was observed in response to BK stimulation.
178	15692059	Treatment of MC with BK (10(-8) M) for 5 min significantly increased the tyrosine phosphorylation of p60src kinase and of p42/p44 MAPK (P < 0.05, n = 4).
179	15692059	Inhibition of src kinase by PP1 (10 microM) inhibited the increase in p42/p44 MAPK activation in response to BK.
180	15692059	Finally, to determine whether BK stimulates CTGF, TGF-betaRII, and collagen I expression via activation of MAPK pathways, MC were pretreated with an inhibitor of p42/p44 MAPK (PD-98059) for 45 min, followed by BK (10(-8) M) stimulation for 24 h.
181	15692059	Selective inhibition of p42/p44 MAPK significantly inhibited the BK-induced increase in CTGF, TGF-betaRII, and collagen I levels.
182	15692059	These findings are the first to demonstrate that BK regulates the expression of CTGF, TGF-betaRII, and collagen I in MC and provide a mechanistic pathway through which B2KR activation may contribute to the development of diabetic nephropathy.
183	15979413	We compared natural as well as bioengineered serotypes of rAAV (rAAV1, rAAV2/Apo, rAAV8) as well as different promoters (chicken beta-actin, human insulin) for their expression in vivo.
184	16177640	We have investigated the effect of transplantation and metabolic environment on the expression of 18S, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), beta-actin, and cyclophilin A genes in pancreatic islets.
185	16177640	The significant variation found in other housekeeping genes, particularly GAPDH and beta-actin, question their use as internal controls in islet grafts.
186	16177640	We have investigated the effect of transplantation and metabolic environment on the expression of 18S, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), beta-actin, and cyclophilin A genes in pancreatic islets.
187	16177640	The significant variation found in other housekeeping genes, particularly GAPDH and beta-actin, question their use as internal controls in islet grafts.
188	16294503	The VEGF-mRNA density showed a increasing tendency by 20% in the diabetic rats compared with the non-diabetic rats (1.0 +/- 0.1 vs 1.2 +/- 0.1 VEGF/beta-actin), and this increase was corrected by 10 mg/kg troxerutin (1.0 +/- 0.1 VEGF/beta-actin), 50 mg/kg troxerutin (0.9 +/- 0.1 VEGF/beta-actin) and Vaccinium myrtillus (1.1 +/- 0.1 VEGF/beta-actin).
189	16298630	We produced transgenic mice in which the human HO-1 transgene driven by chicken beta-actin promoter was expressed in the heart, liver, spleen, lung, kidney, muscle, intestine, and pancreas in Balb/c mice.
190	16443759	Although bone marrow cells expressing GFP under the ubiquitously expressed beta-actin promoter efficiently engrafted the pancreas of normal and hyperglycemic mice, virtually all expressed CD45 and Mac-1/Gr-1, demonstrating that they adopt a hematopoietic rather than beta-cell fate, a finding further substantiated by the complete absence of GFP(+) cells expressing insulin and the beta-cell transcription factors pancreatic duodenal homeobox factor-1 and homeodomain protein.
191	16782585	Proteomics analysis identified a total of eight targets with structural, metabolic and regulatory function, three of which (beta-actin, beta-tubulin and eukaryotic Elongation Factor 1-alpha) were common to both cell lines.
192	18316203	Mice were killed on different days (3, 6 and 12 after skin injury) for measurement of vascular endothelial growth factor (VEGF) mRNA and protein expression, to assess histologically the healing process and to evaluate wound breaking strength and angiogenesis by CD31 immunostaining.
193	18316203	Simvastatin administration in diabetic mice increased VEGF mRNA (simvastatin=4.8+/-0.6n-fold/beta-actin; vehicle=2.3+/-0.4n-fold/beta-actin) and protein expression (simvastatin=5+/-0.7 integrated intensity; vehicle=2.2+/-0.3 integrated intensity) and enhanced nitric oxide wound content at day 6.
194	18316203	Additionally, the statin augmented breaking strength and PECAM-1 immunostaining at day 12.
195	18318806	Mice were killed 3, 6, and 12 days after skin injury to measure vascular endothelial growth factor (VEGF) mRNA expression and protein synthesis, to assay angiogenesis and tissue remodeling through histological evaluation, and to study CD31, Angiopoietin-1 and Transglutaminase-II.
196	18318806	PDRN injection in diabetic mice resulted in an increased VEGF message (vehicle=1.0+/-0.2 n-fold vs. beta-actin; PDRN=1.5+/-0.09 n-fold vs. beta-actin) and protein wound content on day 6 (vehicle=0.3+/-0.07 pg/wound; PDRN=0.9+/-0.1 pg/wound).
197	18780965	In a C57BL/6 mouse model of obesity and T2DM, we characterized the histopathology, gene expression, and insulin and insulin-like growth factor (IGF)-receptor binding in temporal lobe.
198	18780965	These effects were associated with significantly increased levels of tau, IGF-I receptor, insulin receptor substrate-1 (IRS-1), IRS-4, ubiquitin, glial fibrillary acidic protein, and 4-hydroxynonenol, and decreased expression of beta-actin.
199	18802475	After 2-month exercise (treadmill running), the body weight (BW) and expression of calpain 10, mu-calpain, and m-calpain in skeletal muscles were determined by RT-PCR, using beta-actin as internal standard.
200	18837956	The markers were RPE65, retinoschisin, and melanopsin.
201	18837956	Quantitative real-time PCR was used to quantify mRNA for RPE65, retinoschisin, and melanopsin. beta-actin mRNA was used for normalization.
202	18837956	RPE65, retinoschisin, and beta-actin mRNA were detected in 100% of subjects; melanopsin was not detected in either controls or diabetic patients.
203	18837956	Circulating RPE65 mRNA concentration was 63% higher in diabetic patients than in healthy individuals (P= 0.019), whereas retinoschisin showed no change between the two groups.
204	18837956	Both RPE65 and retinoschisin were detectable and demonstrated contrasting trends in diabetics with and without retinopathy.
205	18837956	In combination with rhodopsin, RPE65, and retinoschisin, mRNA may offer a useful tool in developing a blood test for DR.
206	18837956	The markers were RPE65, retinoschisin, and melanopsin.
207	18837956	Quantitative real-time PCR was used to quantify mRNA for RPE65, retinoschisin, and melanopsin. beta-actin mRNA was used for normalization.
208	18837956	RPE65, retinoschisin, and beta-actin mRNA were detected in 100% of subjects; melanopsin was not detected in either controls or diabetic patients.
209	18837956	Circulating RPE65 mRNA concentration was 63% higher in diabetic patients than in healthy individuals (P= 0.019), whereas retinoschisin showed no change between the two groups.
210	18837956	Both RPE65 and retinoschisin were detectable and demonstrated contrasting trends in diabetics with and without retinopathy.
211	18837956	In combination with rhodopsin, RPE65, and retinoschisin, mRNA may offer a useful tool in developing a blood test for DR.
212	19387108	In HFD fed mice, temporal lobe levels of ubiquitin (P<0.001) and 4-hydroxynonenal (P<0.05 or P<0.01) increased, and tau, beta-actin, and choline acetyltransferase levels decreased (P<0.05-P<0.001) with development of NASH.
213	20446237	Using a real-time PCR approach we investigated the mRNA expression levels of Caspase3, Caspase3 s, xIAP, Bad, and beta-actin in a panel of 79 thyroid tumours.
214	21136853	In T1DM with DN, beta-actin and three isoforms of tubulin beta-2 chain, tropomodulin-3, and LASP-1 were decreased, whereas two tubulin beta-4 chain isoforms, one alpha actinin-4 isoform, membrane-organizing extension spike protein (MOESIN), FLJ00279 (corresponding to a fragment of myosin heavy chain, non-muscle type A), vinculin, a tropomyosin isoform, and the macrophage capping protein were increased.
215	23886751	These proteins included prohibitin 1, protein disulphide isomerase A3, beta actin, profilin, aldo-ketoreductase 1 C2, alpha crystallin B and the annexins A1, A5 and A6.
216	23886751	Differences in the abundances of several proteins were confirmed by immunoblotting: i.e., prohibitin 1, protein disulphide isomerase A3, beta actin, profilin and signal transducer and activator of transcription 3 proteins.
217	23886751	These proteins included prohibitin 1, protein disulphide isomerase A3, beta actin, profilin, aldo-ketoreductase 1 C2, alpha crystallin B and the annexins A1, A5 and A6.
218	23886751	Differences in the abundances of several proteins were confirmed by immunoblotting: i.e., prohibitin 1, protein disulphide isomerase A3, beta actin, profilin and signal transducer and activator of transcription 3 proteins.