Ignet

Gene Information

Gene symbol: GDNF

Gene name: glial cell derived neurotrophic factor

HGNC ID: 4232

Synonyms: ATF1, ATF2, HFB1-GDNF

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	BDNF	1 hits
3	BMP4	1 hits
4	CD28	1 hits
5	CHAT	1 hits
6	CNTF	1 hits
7	ELK1	1 hits
8	EPO	1 hits
9	FGF2	1 hits
10	HSPB1	1 hits
11	IFNG	1 hits
12	IGF1	1 hits
13	IGF2	1 hits
14	IL1B	1 hits
15	IL2	1 hits
16	IL4	1 hits
17	INS	1 hits
18	ITGAM	1 hits
19	JUN	1 hits
20	MAPK1	1 hits
21	MAPK14	1 hits
22	NEUROD1	1 hits
23	NEUROG3	1 hits
24	NGF	1 hits
25	NR4A1	1 hits
26	NRTN	1 hits
27	NT3	1 hits
28	NTF3	1 hits
29	NTF4	1 hits
30	NUDT6	1 hits
31	PAX4	1 hits
32	PAX6	1 hits
33	PDX1	1 hits
34	PIK3CA	1 hits
35	RAPGEF5	1 hits
36	RET	1 hits
37	SHH	1 hits
38	SOX9	1 hits
39	WNT11	1 hits

Related Sentences

#	PMID	Sentence
1	8580713	Thus, the effect of axotomy on neuropeptide expression in dorsal root ganglion cells is partially reversed by nerve growth factor treatment, and the effect on choline acetyltransferase expression in motoneurones is partially reversed by glial-derived neurotrophic factor, neurotrophin-4/5 and brain-derived neurotrophic factor.
2	8580713	Nerve growth factor also ameliorates some of the changes seen in sensory neurones in animal models of diabetic neuropathy and small fibre cytostatic drug neuropathy, whereas neurotrophin-3 has been found to reverse some changes in large sensory neurones associated with cisplatin neurotoxicity.
3	10201899	p38 mitogen-activated protein kinase mediates signal integration of TCR/CD28 costimulation in primary murine T cells.
4	10201899	In contrast to that reported for human Jurkat T cells, we found that p38 MAPK, but not Jun NH2-terminal kinase (JNK), is weakly activated upon stimulation with either anti-CD3 or anti-CD28 in murine thymocytes and splenic T cells.
5	10201899	However, p38 MAPK is activated strongly and synergistically by either CD3/CD28 coligation or PMA/Ca2+ ionophore stimulation, which mimics TCR-CD3/CD28-mediated signaling.
6	10201899	Activation of p38 MAPK correlates closely with the stimulation of T cell proliferation.
7	10201899	T cell proliferation and production of IL-2, IL-4, and IFN-gamma induced by both CD3 and CD3/CD28 ligation and the nuclear expression of the c-Jun and ATF-2 proteins are each blocked by the p38 MAPK inhibitor SB203580.
8	10201899	Our findings demonstrate that p38 MAPK 1) plays an important role in signal integration during costimulation of primary mouse T cells, 2) may be involved in the induction of c-Jun activation and augmentation of AP-1 transcriptional activity, and 3) regulates whether T cells enter a state of functional unresponsiveness.
9	10219753	These include the neurotrophins (nerve growth factor, brain derived neurotrophic factor, neurotrophin-3, neurotrophin-4/5), the insulin like growth factors, ciliary neurotrophic factor, and glial cell derived neurotrophic factor and its related proteins.
10	10484043	Among the most promising are members of the neurotrophin gene family (nerve growth factor [NGF], brain-derived neurotrophic factor, neurotrophin [NT]-3, and NT-4/5), insulin-like growth factor (IGF)-I and IGF-II, and glial cell-derived neurotrophic factor.
11	10903806	Activation of extracellular signal-regulated kinase (ERK)1/2 contributes to cytokine-induced apoptosis in purified rat pancreatic beta-cells.
12	10903806	It has been reported recently that interleukin-1 beta (IL-1 beta) induces activation of the mitogen-activated protein kinases (MAPK) p38 and ERK1/2 in neonatal rat islets.
13	10903806	Since these kinases may participate in cytokine-induced apoptosis, we evaluated whether cytokines induce activation of MAPKs in FACS-purified primary rat beta-cells, and whether blockers of p38 and/or ERK1/2 prevent beta-cell death.
14	10903806	IL-1 beta, but not interferon-gamma (IFN-gamma), caused phosphorylation of the substrates Elk-1, ATF-2 and hsp25, and the phosphorylation of both Elk-1 and hsp25 were decreased by the p38 blocker SB203580 (p38i) and the MAPK/ERK blocker PD 098059 (MEKi).
15	10903806	When added together, p38i and MEKi decreased IL-1 beta-induced nitrite production over 24 hours by 60%, but did not affect IL-1 beta-induced manganese superoxide dismutase (MnSOD) mRNA expression.
16	10903806	To test the effects of MAPK inhibitors on beta-cell death by necrosis or apoptosis, these cells were exposed for 6 or 9 days to IL-1 beta + IFN-gamma.
17	10903806	We conclude that IL-1 beta induces activation of both p38 and ERK1/2, and that ERK1/2 contributes to the pro-apoptotic effects of the cytokine in primary beta-cells.
18	10969830	The c-Jun amino-terminal kinase pathway is preferentially activated by interleukin-1 and controls apoptosis in differentiating pancreatic beta-cells.
19	10969830	To characterize the differentiation events that selectively target insulin-producing cells to interleukin (IL)-1beta-induced apoptosis, we studied IL-1beta signaling via mitogen-activated protein kinase (MAPK) and stress-activated protein kinase in 2 pancreatic endocrine cell lines.
20	10969830	We studied the glucagon-secreting AN-glu cell line and the insulin and the islet amyloid polypeptide-producing beta-cell line (AN-ins cells), which is derived by stable transfection of AN-glu cells with the transcription factor pancreatic duodenal homeobox factor-1.
21	10969830	This increased sensitivity was not associated with a more pronounced IL-l-induced nitric oxide production in AN-ins cells, but it correlated with a more marked activation of the 3 MAPKs extracellular signal-regulated kinases (ERKs)-1/2, c-Jun NH2-terminal kinase (JNK), and p38 MAPK (p38).
22	10969830	This led to increased phosphorylation of the transcription factors c-Jun, Elk-1, and ATF2 and of heat shock protein 25.
23	10969830	Inhibition of ERK-1/2 and p38 did not prevent but aggravated IL-1beta-induced cell death.
24	10969830	Cell death could be elicited by overexpressing the catalytic domain of MAPK kinase kinase 1, a specific activator of JNK and nuclear factor-kappaB, which does not recruit ERK-1/2 or p38.
25	10969830	Coactivation of ERK-1/2 with JNK did not prevent apoptosis.
26	10969830	In conclusion, increased MAPK signaling in response to IL-1beta may represent a novel molecular marker of beta-cell differentiation.
27	11161605	The peptidergic population responds to nerve growth factor (NGF), while the nonpeptidergic DRG neurons postnatally switch their dependency from NGF to glial cell line-derived neurotrophic factor (GDNF).
28	11161605	In contrast, NGF-responsive CGRP-immunoreactive (ir) axons showed no or only a slight decrease in spinal terminations.
29	11161605	To test whether GDNF or NGF could restore spinal deficits in nonpeptidergic afferents, STZ-treated mice were treated intrathecally for 2 weeks with NGF or GDNF.
30	11161605	The peptidergic population responds to nerve growth factor (NGF), while the nonpeptidergic DRG neurons postnatally switch their dependency from NGF to glial cell line-derived neurotrophic factor (GDNF).
31	11161605	In contrast, NGF-responsive CGRP-immunoreactive (ir) axons showed no or only a slight decrease in spinal terminations.
32	11161605	To test whether GDNF or NGF could restore spinal deficits in nonpeptidergic afferents, STZ-treated mice were treated intrathecally for 2 weeks with NGF or GDNF.
33	11340638	Disruption of the Nurr1 gene in mice by homologous recombination abolishes synthesis of dopamine (DA) and expression of DA biosynthetic enzymes, including tyrosine hydroxylase (TH), in the ventral midbrain without affecting the synthesis of DA in other areas of the brain.
34	11340638	No change in TH expression was observed in the presence of glial cell line-derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF), or DA alone or in combination.
35	12618126	Cutaneous innervation was quantified in the hindlimb skin using antibodies that label nerve growth factor- (NGF) responsive (CGRP), glial cell line-derived neurotrophic factor (GDNF)/neurturin (NTN) -responsive (P2X(3)), or all cutaneous axons (PGP 9.5).
36	12618126	Qualitative assessment of mRNAs for NGF, GDNF, and NTN demonstrated that these mRNAs were expressed in hindlimb flank and footpad skin from diabetic mice.
37	12618126	Next, diabetic mice were then treated intrathecally for 2 weeks with NGF, GDNF, or NTN.
38	12618126	In comparison, GDNF and NTN treatment increased cutaneous innervation and axon branching.
39	12618126	Importantly, intrathecal treatment using GDNF or NTN strongly stimulated axon growth and branching, suggesting that administration of these trophic factors can improve cutaneous innervation deficits caused by diabetes.
40	12618126	Cutaneous innervation was quantified in the hindlimb skin using antibodies that label nerve growth factor- (NGF) responsive (CGRP), glial cell line-derived neurotrophic factor (GDNF)/neurturin (NTN) -responsive (P2X(3)), or all cutaneous axons (PGP 9.5).
41	12618126	Qualitative assessment of mRNAs for NGF, GDNF, and NTN demonstrated that these mRNAs were expressed in hindlimb flank and footpad skin from diabetic mice.
42	12618126	Next, diabetic mice were then treated intrathecally for 2 weeks with NGF, GDNF, or NTN.
43	12618126	In comparison, GDNF and NTN treatment increased cutaneous innervation and axon branching.
44	12618126	Importantly, intrathecal treatment using GDNF or NTN strongly stimulated axon growth and branching, suggesting that administration of these trophic factors can improve cutaneous innervation deficits caused by diabetes.
45	12618126	Cutaneous innervation was quantified in the hindlimb skin using antibodies that label nerve growth factor- (NGF) responsive (CGRP), glial cell line-derived neurotrophic factor (GDNF)/neurturin (NTN) -responsive (P2X(3)), or all cutaneous axons (PGP 9.5).
46	12618126	Qualitative assessment of mRNAs for NGF, GDNF, and NTN demonstrated that these mRNAs were expressed in hindlimb flank and footpad skin from diabetic mice.
47	12618126	Next, diabetic mice were then treated intrathecally for 2 weeks with NGF, GDNF, or NTN.
48	12618126	In comparison, GDNF and NTN treatment increased cutaneous innervation and axon branching.
49	12618126	Importantly, intrathecal treatment using GDNF or NTN strongly stimulated axon growth and branching, suggesting that administration of these trophic factors can improve cutaneous innervation deficits caused by diabetes.
50	12618126	Cutaneous innervation was quantified in the hindlimb skin using antibodies that label nerve growth factor- (NGF) responsive (CGRP), glial cell line-derived neurotrophic factor (GDNF)/neurturin (NTN) -responsive (P2X(3)), or all cutaneous axons (PGP 9.5).
51	12618126	Qualitative assessment of mRNAs for NGF, GDNF, and NTN demonstrated that these mRNAs were expressed in hindlimb flank and footpad skin from diabetic mice.
52	12618126	Next, diabetic mice were then treated intrathecally for 2 weeks with NGF, GDNF, or NTN.
53	12618126	In comparison, GDNF and NTN treatment increased cutaneous innervation and axon branching.
54	12618126	Importantly, intrathecal treatment using GDNF or NTN strongly stimulated axon growth and branching, suggesting that administration of these trophic factors can improve cutaneous innervation deficits caused by diabetes.
55	12618126	Cutaneous innervation was quantified in the hindlimb skin using antibodies that label nerve growth factor- (NGF) responsive (CGRP), glial cell line-derived neurotrophic factor (GDNF)/neurturin (NTN) -responsive (P2X(3)), or all cutaneous axons (PGP 9.5).
56	12618126	Qualitative assessment of mRNAs for NGF, GDNF, and NTN demonstrated that these mRNAs were expressed in hindlimb flank and footpad skin from diabetic mice.
57	12618126	Next, diabetic mice were then treated intrathecally for 2 weeks with NGF, GDNF, or NTN.
58	12618126	In comparison, GDNF and NTN treatment increased cutaneous innervation and axon branching.
59	12618126	Importantly, intrathecal treatment using GDNF or NTN strongly stimulated axon growth and branching, suggesting that administration of these trophic factors can improve cutaneous innervation deficits caused by diabetes.
60	14636817	To evaluate whether neurotrophin treatment could normalize the sensory deficits, nerve growth factor (NGF) or glial cell line-derived neurotrophic factor (GDNF) was administered intrathecally to diabetic mice for 3 weeks.
61	14636817	Neurotrophin-treated mice were also compared to mice that received insulin for 3 weeks.
62	14636817	Both NGF and insulin treatment significantly restored mechanical and chemogenic behavioral responses of diabetic mice.
63	14636817	Furthermore, these studies show that dorsal root ganglion neurons in diabetic mice are responsive to treatment with either NGF or GDNF; however, these 2 neurotrophins differ in their ability to affect distinct somatosensations.
64	14636817	To evaluate whether neurotrophin treatment could normalize the sensory deficits, nerve growth factor (NGF) or glial cell line-derived neurotrophic factor (GDNF) was administered intrathecally to diabetic mice for 3 weeks.
65	14636817	Neurotrophin-treated mice were also compared to mice that received insulin for 3 weeks.
66	14636817	Both NGF and insulin treatment significantly restored mechanical and chemogenic behavioral responses of diabetic mice.
67	14636817	Furthermore, these studies show that dorsal root ganglion neurons in diabetic mice are responsive to treatment with either NGF or GDNF; however, these 2 neurotrophins differ in their ability to affect distinct somatosensations.
68	15855316	Neurturin signaling via glial cell line-derived neurotrophic factor family receptor alpha2 (GFRalpha2) has been demonstrated to be essential for the development of subsets of parasympathetic and enteric neurons.
69	15855316	In the GFRalpha2-KO mice, however, pancreatic polypeptide and insulin responses were completely lost and glucagon response was markedly impaired.
70	16453015	In this issue of the JCI, Anitha et al. report apoptosis of rodent enteric neurons under hyperglycemic conditions, both in vitro and in vivo, associated with impaired PI3K activity and preventable by glial cell line-derived neurotrophic factor.
71	16453021	GDNF rescues hyperglycemia-induced diabetic enteric neuropathy through activation of the PI3K/Akt pathway.
72	16453021	Exposure to 20 mM glucose resulted in decreased Akt phosphorylation and enhanced nuclear translocation of forkhead box O3a (FOXO3a).
73	16453021	The pathophysiological effects of hyperglycemia (apoptosis, reduced Akt phosphorylation, loss of inhibitory neurons, motility changes) were reversed in diabetic glial fibrillary acidic protein-GDNF (GFAP-GDNF) Tg mice.
74	16914836	Genes such as GDNF, BDNF and integrin-alpha-M were up-regulated, while immediate-early-gene-transcription-factor NGF-IB and metallothionein-1/2 were down-regulated in the cortex of streptozotocin-treated rats.
75	16914836	Conversely, NGF-IB, GDNF and BDNF mRNA expression did not alter in the striatum and cerebellum.
76	16914836	Genes such as GDNF, BDNF and integrin-alpha-M were up-regulated, while immediate-early-gene-transcription-factor NGF-IB and metallothionein-1/2 were down-regulated in the cortex of streptozotocin-treated rats.
77	16914836	Conversely, NGF-IB, GDNF and BDNF mRNA expression did not alter in the striatum and cerebellum.
78	20042376	And the expression of glia cell-derived neurotrophic factor (GDNF), neurotrophin 3 (NT-3) and nerve growth factor (NGF) was analyzed by real-time PCR and western blot.
79	20042376	Moreover, mRNA and protein analysis indicated that the levels of GDNF, NT-3 and NGF were down-regulated in diabetic rats.
80	20042376	And the expression of glia cell-derived neurotrophic factor (GDNF), neurotrophin 3 (NT-3) and nerve growth factor (NGF) was analyzed by real-time PCR and western blot.
81	20042376	Moreover, mRNA and protein analysis indicated that the levels of GDNF, NT-3 and NGF were down-regulated in diabetic rats.
82	20448145	Glial cell line-derived neurotrophic factor enhances neurogenin3 gene expression and beta-cell proliferation in the developing mouse pancreas.
83	20448145	In this study we examined the influence of GDNF on the expression of neurogenin3 (Ngn3) and other transcription factors implicated in early beta-cell development, as well as on beta-cell proliferation during embryonic and early postnatal mouse pancreas development.
84	20448145	Embryonic day 15.5 (E15.5) mouse pancreatic tissue when exposed to GDNF for 24 h showed higher Ngn3, pancreatic and duodenal homeobox gene 1 (Pdx1), neuroD1/beta(2), paired homeobox gene 4 (Pax4), and insulin mRNA expression than tissue exposed to vehicle only.
85	20448145	Transgenic expression of GDNF in mouse pancreata was associated with increased numbers of Ngn3-expressing pancreatic cells and higher beta-cell mass at embryonic day 18 (E18), as well as higher beta-cell proliferation and Pdx1 expression in beta-cells at E18 and postnatal day 1.
86	20448145	In the HIT-T15 beta-cell line, GDNF enhanced the expression of Pax6.
87	20448145	Chromatin immunoprecipitation studies using the HIT-T15 beta-cell line demonstrated that GDNF can influence Pdx1 gene expression by enhancing the binding of Sox9 and neuroD1/beta(2) to the Pdx1 promoter.
88	20448145	Glial cell line-derived neurotrophic factor enhances neurogenin3 gene expression and beta-cell proliferation in the developing mouse pancreas.
89	20448145	In this study we examined the influence of GDNF on the expression of neurogenin3 (Ngn3) and other transcription factors implicated in early beta-cell development, as well as on beta-cell proliferation during embryonic and early postnatal mouse pancreas development.
90	20448145	Embryonic day 15.5 (E15.5) mouse pancreatic tissue when exposed to GDNF for 24 h showed higher Ngn3, pancreatic and duodenal homeobox gene 1 (Pdx1), neuroD1/beta(2), paired homeobox gene 4 (Pax4), and insulin mRNA expression than tissue exposed to vehicle only.
91	20448145	Transgenic expression of GDNF in mouse pancreata was associated with increased numbers of Ngn3-expressing pancreatic cells and higher beta-cell mass at embryonic day 18 (E18), as well as higher beta-cell proliferation and Pdx1 expression in beta-cells at E18 and postnatal day 1.
92	20448145	In the HIT-T15 beta-cell line, GDNF enhanced the expression of Pax6.
93	20448145	Chromatin immunoprecipitation studies using the HIT-T15 beta-cell line demonstrated that GDNF can influence Pdx1 gene expression by enhancing the binding of Sox9 and neuroD1/beta(2) to the Pdx1 promoter.
94	20448145	Glial cell line-derived neurotrophic factor enhances neurogenin3 gene expression and beta-cell proliferation in the developing mouse pancreas.
95	20448145	In this study we examined the influence of GDNF on the expression of neurogenin3 (Ngn3) and other transcription factors implicated in early beta-cell development, as well as on beta-cell proliferation during embryonic and early postnatal mouse pancreas development.
96	20448145	Embryonic day 15.5 (E15.5) mouse pancreatic tissue when exposed to GDNF for 24 h showed higher Ngn3, pancreatic and duodenal homeobox gene 1 (Pdx1), neuroD1/beta(2), paired homeobox gene 4 (Pax4), and insulin mRNA expression than tissue exposed to vehicle only.
97	20448145	Transgenic expression of GDNF in mouse pancreata was associated with increased numbers of Ngn3-expressing pancreatic cells and higher beta-cell mass at embryonic day 18 (E18), as well as higher beta-cell proliferation and Pdx1 expression in beta-cells at E18 and postnatal day 1.
98	20448145	In the HIT-T15 beta-cell line, GDNF enhanced the expression of Pax6.
99	20448145	Chromatin immunoprecipitation studies using the HIT-T15 beta-cell line demonstrated that GDNF can influence Pdx1 gene expression by enhancing the binding of Sox9 and neuroD1/beta(2) to the Pdx1 promoter.
100	20448145	Glial cell line-derived neurotrophic factor enhances neurogenin3 gene expression and beta-cell proliferation in the developing mouse pancreas.
101	20448145	In this study we examined the influence of GDNF on the expression of neurogenin3 (Ngn3) and other transcription factors implicated in early beta-cell development, as well as on beta-cell proliferation during embryonic and early postnatal mouse pancreas development.
102	20448145	Embryonic day 15.5 (E15.5) mouse pancreatic tissue when exposed to GDNF for 24 h showed higher Ngn3, pancreatic and duodenal homeobox gene 1 (Pdx1), neuroD1/beta(2), paired homeobox gene 4 (Pax4), and insulin mRNA expression than tissue exposed to vehicle only.
103	20448145	Transgenic expression of GDNF in mouse pancreata was associated with increased numbers of Ngn3-expressing pancreatic cells and higher beta-cell mass at embryonic day 18 (E18), as well as higher beta-cell proliferation and Pdx1 expression in beta-cells at E18 and postnatal day 1.
104	20448145	In the HIT-T15 beta-cell line, GDNF enhanced the expression of Pax6.
105	20448145	Chromatin immunoprecipitation studies using the HIT-T15 beta-cell line demonstrated that GDNF can influence Pdx1 gene expression by enhancing the binding of Sox9 and neuroD1/beta(2) to the Pdx1 promoter.
106	20448145	Glial cell line-derived neurotrophic factor enhances neurogenin3 gene expression and beta-cell proliferation in the developing mouse pancreas.
107	20448145	In this study we examined the influence of GDNF on the expression of neurogenin3 (Ngn3) and other transcription factors implicated in early beta-cell development, as well as on beta-cell proliferation during embryonic and early postnatal mouse pancreas development.
108	20448145	Embryonic day 15.5 (E15.5) mouse pancreatic tissue when exposed to GDNF for 24 h showed higher Ngn3, pancreatic and duodenal homeobox gene 1 (Pdx1), neuroD1/beta(2), paired homeobox gene 4 (Pax4), and insulin mRNA expression than tissue exposed to vehicle only.
109	20448145	Transgenic expression of GDNF in mouse pancreata was associated with increased numbers of Ngn3-expressing pancreatic cells and higher beta-cell mass at embryonic day 18 (E18), as well as higher beta-cell proliferation and Pdx1 expression in beta-cells at E18 and postnatal day 1.
110	20448145	In the HIT-T15 beta-cell line, GDNF enhanced the expression of Pax6.
111	20448145	Chromatin immunoprecipitation studies using the HIT-T15 beta-cell line demonstrated that GDNF can influence Pdx1 gene expression by enhancing the binding of Sox9 and neuroD1/beta(2) to the Pdx1 promoter.
112	20448145	Glial cell line-derived neurotrophic factor enhances neurogenin3 gene expression and beta-cell proliferation in the developing mouse pancreas.
113	20448145	In this study we examined the influence of GDNF on the expression of neurogenin3 (Ngn3) and other transcription factors implicated in early beta-cell development, as well as on beta-cell proliferation during embryonic and early postnatal mouse pancreas development.
114	20448145	Embryonic day 15.5 (E15.5) mouse pancreatic tissue when exposed to GDNF for 24 h showed higher Ngn3, pancreatic and duodenal homeobox gene 1 (Pdx1), neuroD1/beta(2), paired homeobox gene 4 (Pax4), and insulin mRNA expression than tissue exposed to vehicle only.
115	20448145	Transgenic expression of GDNF in mouse pancreata was associated with increased numbers of Ngn3-expressing pancreatic cells and higher beta-cell mass at embryonic day 18 (E18), as well as higher beta-cell proliferation and Pdx1 expression in beta-cells at E18 and postnatal day 1.
116	20448145	In the HIT-T15 beta-cell line, GDNF enhanced the expression of Pax6.
117	20448145	Chromatin immunoprecipitation studies using the HIT-T15 beta-cell line demonstrated that GDNF can influence Pdx1 gene expression by enhancing the binding of Sox9 and neuroD1/beta(2) to the Pdx1 promoter.
118	21264951	The number of microglia time dependently increased at demyelinative lesion sites, proliferated, and expressed tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, inducible nitric oxide synthase, and MMP2, 9, and 12 at the early phase.
119	21264951	The number of astrocytes time dependently increased around demyelinative lesions, extended processes to lesions, proliferated, and expressed nerve growth factor and glial cell line-derived neurotrophic factor at the late phase.
120	21903675	Embryonic day 12.5 kidneys revealed an almost complete absence of basement membrane proteins and reduced levels of α6 integrin and FGF2. mRNA levels for fibroblast growth factor 2 (FGF2) and mediators of the GDNF/RET and WNT11 signaling pathway were also decreased.
121	22266674	These results suggest that Müller cells can synthesize GDNF and GFRs under high glucose conditions, and GDNF may play important role in protecting Müller cells during the early stage of diabetic retinopathy.
122	22266674	The difference in GFRs expression indicated that GDNF and neurturin may exert different effects on Müller cells under high glucose circumstance.
123	22266674	These results suggest that Müller cells can synthesize GDNF and GFRs under high glucose conditions, and GDNF may play important role in protecting Müller cells during the early stage of diabetic retinopathy.
124	22266674	The difference in GFRs expression indicated that GDNF and neurturin may exert different effects on Müller cells under high glucose circumstance.
125	22374754	Glial cell line-derived neurotrophic factor and Ret proto-oncogene gene expression was decreased in both MD-WLWL and MD-LWLW fetuses, whereas increased bone morphogenetic protein 4 and decreased Sonic hedgehog homolog expression was found only in MD-LWLW fetuses.
126	23735822	As a metabolic disorder depression has been associated with obesity, diabetes, insulin sensitivity, neuropeptide Y, glucose regulation, poor glycemic control, glucagone-like peptide-1, cholezystokinin, ghrelin, leptin, the endocannabinoid system, insulin-like growth factor and gastrin-releasing peptide.
127	23735822	Additionally blood coagulation, fibrinolysis, D-dimers, plasminogen activator inhibitor-1 protein, platelet activation, VEGF, plasma nitric oxide and its synthase are changed in depressed patients.
128	23735822	As an endocrinological and stress disorder depression has been connected with the concentration of free T4, TSH, CRH, arginine vasopressin, corticotrophin, corticosteroid release and ACTH.
129	23735822	Depression as an inflammatory disorder is mediated by pro-inflammatory cytokines, interleukin-1, interleukin-6, TNF-alpha, soluble interleukin-2 receptors, interferon-alpha, interleukin 8, interleukin-10, hs-CRP, acute phase proteins, haptoglobin, toll like receptor 4, interleukin-1beta, mammalian target of rapamycin pathway, substance P, cyclooxygenase-2, prostaglandin-E2, lipid peroxidation levels and acid sphingomyelinase.
130	23735822	The neurodegenerative hypothesis of depression explains decreased hippocampal volumes in depressed patients and changes of neurotrophic support by BDNF, erythropoietin, GDNF, FGF-2, NT3, NGF and growth hormone.
131	23735822	Hence, GABA, AMPA, EAAT, NMDA- and metabotropic glutamate receptors (mGluR1 to mGluR8) have gained interest in depression recently.