Ignet

Gene Information

Gene symbol: GLI1

Gene name: GLI family zinc finger 1

HGNC ID: 4317

Related Genes

#	Gene Symbol	Number of hits
1	AKR1B1	1 hits
2	CHRDL1	1 hits
3	GIP	1 hits
4	GLIS3	1 hits
5	GLO1	1 hits
6	INS	1 hits
7	SUFU	1 hits
8	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	488570	The reduction of GIP or GLI secretion may, therefore, be partly responsible for the smaller rise in plasma insulin observed in normal volunteers when guar is added to meals.
2	9437909	Glibenclamide (GLI) or chlorpropamide (CHL) was chosen as a principal agent and ointments were prepared by mixing 5% of GLI or CHL with a FAPG ointment base.
3	9437909	When the ointments were applied on the back of male Wistar rats and the plasma glucose level was measured, both CHL and GLI ointments gave lower blood glucose levels than the control (FAPG base).
4	9437909	Glibenclamide (GLI) or chlorpropamide (CHL) was chosen as a principal agent and ointments were prepared by mixing 5% of GLI or CHL with a FAPG ointment base.
5	9437909	When the ointments were applied on the back of male Wistar rats and the plasma glucose level was measured, both CHL and GLI ointments gave lower blood glucose levels than the control (FAPG base).
6	16715098	Here, we show that this syndrome results from mutations in GLIS3, encoding GLI similar 3, a recently identified transcription factor.
7	18263616	The Krüppel-like zinc finger protein Gli-similar 3 (Glis3) plays a critical role in pancreatic development and has been implicated in a syndrome with neonatal diabetes and hypothyroidism (NDH).
8	18720345	The intake of these compounds significantly and dose-dependently decreased the levels of plasma glycated hemoglobin (HbA1c), renal carboxymethyllysine and urinary glycated albumin (p < 0.05).
9	18720345	SEC or SPC intake significantly and dose-dependently diminished renal aldose reductase (AR) activity and enhanced glyoxalase I (GLI) activity (p < 0.05); also significantly decreased renal sorbitol and fructose concentrations (p < 0.05).
10	18720345	The intake of SEC or SPC significantly lowered renal VEGF level (p < 0.05), and caused dose-dependent downregulation in AR mRNA expression, and upregulation in GLI mRNA expression (p < 0.05).
11	18720345	The intake of these compounds significantly and dose-dependently decreased the levels of plasma glycated hemoglobin (HbA1c), renal carboxymethyllysine and urinary glycated albumin (p < 0.05).
12	18720345	SEC or SPC intake significantly and dose-dependently diminished renal aldose reductase (AR) activity and enhanced glyoxalase I (GLI) activity (p < 0.05); also significantly decreased renal sorbitol and fructose concentrations (p < 0.05).
13	18720345	The intake of SEC or SPC significantly lowered renal VEGF level (p < 0.05), and caused dose-dependent downregulation in AR mRNA expression, and upregulation in GLI mRNA expression (p < 0.05).
14	19805515	Transcription factor Glis3, a novel critical player in the regulation of pancreatic beta-cell development and insulin gene expression.
15	19805515	In this study, we report that the Krüppel-like zinc finger transcription factor Gli-similar 3 (Glis3) is induced during the secondary transition of pancreatic development, a stage of cell lineage specification and extensive patterning, and that Glis3(zf/zf) mutant mice develop neonatal diabetes, evidenced by hyperglycemia and hypoinsulinemia.
16	19805515	Gene expression profiling and immunofluorescent staining demonstrated that the expression of pancreatic hormones and several transcription factors important in endocrine cell development, including Ngn3, MafA, and Pdx1, were significantly decreased in the developing pancreata of Glis3(zf/zf) mutant mice.
17	19805515	The population of pancreatic progenitors appears not to be greatly affected in Glis3(zf/zf) mutant mice; however, the number of neurogenin 3 (Ngn3)-positive endocrine cell progenitors is significantly reduced.
18	19805515	In addition, we provide evidence that Glis3 regulates insulin gene expression through two Glis-binding sites in its proximal promoter, indicating that Glis3 also regulates beta-cell function.
19	21543335	Modulation of the transactivation function and stability of Krüppel-like zinc finger protein Gli-similar 3 (Glis3) by Suppressor of Fused.
20	21543335	Recently, Glis3 has been linked to both type I and type II diabetes and shown to positively regulate insulin gene expression.
21	21543335	In this study, we have identified a region within the N terminus of Glis3 that shares high levels of homology with the Cubitus interruptus (Ci)/Gli family of proteins.
22	21543335	We demonstrated that Glis3 interacts with Suppressor of Fused (SUFU), which involves a VYGHF motif located within this conserved region.
23	21543335	We further showed that SUFU is able to inhibit the activation of the insulin promoter by Glis3 but not the activation by a Glis3 mutant deficient in its ability to bind SUFU, suggesting that the inhibitory effect is dependent on the interaction between the two proteins.
24	21543335	Exogenous SUFU did not affect the nuclear localization of Glis3; however, Glis3 promoted the nuclear accumulation of SUFU.
25	21543335	Additionally, we demonstrated that SUFU stabilizes Glis3 in part by antagonizing the Glis3 association with a Cullin 3-based E3 ubiquitin ligase that promotes the ubiquitination and degradation of Glis3.
26	21543335	This is the first reported instance of Glis3 interacting with SUFU and suggests a novel role for SUFU in the modulation of Glis3 signaling.
27	21543335	Given the critical role of Glis3 in pancreatic β-cell generation and maintenance, the elevated Glis3 expression in several cancers, and the established role of SUFU as a tumor suppressor, these data provide further insight into Glis3 regulation and its function in development and disease.
28	21543335	Modulation of the transactivation function and stability of Krüppel-like zinc finger protein Gli-similar 3 (Glis3) by Suppressor of Fused.
29	21543335	Recently, Glis3 has been linked to both type I and type II diabetes and shown to positively regulate insulin gene expression.
30	21543335	In this study, we have identified a region within the N terminus of Glis3 that shares high levels of homology with the Cubitus interruptus (Ci)/Gli family of proteins.
31	21543335	We demonstrated that Glis3 interacts with Suppressor of Fused (SUFU), which involves a VYGHF motif located within this conserved region.
32	21543335	We further showed that SUFU is able to inhibit the activation of the insulin promoter by Glis3 but not the activation by a Glis3 mutant deficient in its ability to bind SUFU, suggesting that the inhibitory effect is dependent on the interaction between the two proteins.
33	21543335	Exogenous SUFU did not affect the nuclear localization of Glis3; however, Glis3 promoted the nuclear accumulation of SUFU.
34	21543335	Additionally, we demonstrated that SUFU stabilizes Glis3 in part by antagonizing the Glis3 association with a Cullin 3-based E3 ubiquitin ligase that promotes the ubiquitination and degradation of Glis3.
35	21543335	This is the first reported instance of Glis3 interacting with SUFU and suggests a novel role for SUFU in the modulation of Glis3 signaling.
36	21543335	Given the critical role of Glis3 in pancreatic β-cell generation and maintenance, the elevated Glis3 expression in several cancers, and the established role of SUFU as a tumor suppressor, these data provide further insight into Glis3 regulation and its function in development and disease.
37	23927931	The Krüppel-like protein Gli-similar 3 (Glis3) functions as a key regulator of insulin transcription.
38	23927931	Recently, the Krüppel-like transcription factor, Gli-similar 3 (Glis3), was shown to bind the insulin (INS) promoter and positively influence insulin transcription.
39	23927931	In this report, we examined in detail the synergistic activation of insulin transcription by Glis3 with coregulators, CREB-binding protein (CBP)/p300, pancreatic and duodenal homeobox 1 (Pdx1), neuronal differentiation 1 (NeuroD1), and v-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MafA).
40	23927931	Our data show that Glis3 expression, the binding of Glis3 to GlisBS, and its recruitment of CBP are required for optimal activation of the insulin promoter in pancreatic β-cells not only by Glis3, but also by Pdx1, MafA, and NeuroD1.
41	23927931	Mutations in the GlisBS or small interfering RNA-directed knockdown of GLIS3 diminished insulin promoter activation by Pdx1, NeuroD1, and MafA, and neither Pdx1 nor MafA was able to stably associate with the insulin promoter when the GlisBS were mutated.
42	23927931	In addition, a GlisBS mutation in the INS promoter implicated in the development of neonatal diabetes similarly abated activation by Pdx1, NeuroD1, and MafA that could be reversed by increased expression of exogenous Glis3.
43	23927931	We therefore propose that recruitment of CBP/p300 by Glis3 provides a scaffold for the formation of a larger transcriptional regulatory complex that stabilizes the binding of Pdx1, NeuroD1, and MafA complexes to their respective binding sites within the insulin promoter.
44	23927931	Taken together, these results indicate that Glis3 plays a pivotal role in the transcriptional regulation of insulin and may serve as an important therapeutic target for the treatment of diabetes.
45	23927931	The Krüppel-like protein Gli-similar 3 (Glis3) functions as a key regulator of insulin transcription.
46	23927931	Recently, the Krüppel-like transcription factor, Gli-similar 3 (Glis3), was shown to bind the insulin (INS) promoter and positively influence insulin transcription.
47	23927931	In this report, we examined in detail the synergistic activation of insulin transcription by Glis3 with coregulators, CREB-binding protein (CBP)/p300, pancreatic and duodenal homeobox 1 (Pdx1), neuronal differentiation 1 (NeuroD1), and v-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MafA).
48	23927931	Our data show that Glis3 expression, the binding of Glis3 to GlisBS, and its recruitment of CBP are required for optimal activation of the insulin promoter in pancreatic β-cells not only by Glis3, but also by Pdx1, MafA, and NeuroD1.
49	23927931	Mutations in the GlisBS or small interfering RNA-directed knockdown of GLIS3 diminished insulin promoter activation by Pdx1, NeuroD1, and MafA, and neither Pdx1 nor MafA was able to stably associate with the insulin promoter when the GlisBS were mutated.
50	23927931	In addition, a GlisBS mutation in the INS promoter implicated in the development of neonatal diabetes similarly abated activation by Pdx1, NeuroD1, and MafA that could be reversed by increased expression of exogenous Glis3.
51	23927931	We therefore propose that recruitment of CBP/p300 by Glis3 provides a scaffold for the formation of a larger transcriptional regulatory complex that stabilizes the binding of Pdx1, NeuroD1, and MafA complexes to their respective binding sites within the insulin promoter.
52	23927931	Taken together, these results indicate that Glis3 plays a pivotal role in the transcriptional regulation of insulin and may serve as an important therapeutic target for the treatment of diabetes.