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GLIS family zinc finger 3

GLIS3, GLI-similar 3
This gene is a member of the GLI-similar zinc finger protein family and encodes a nuclear protein with five C2H2-type zinc finger domains. This protein functions as both a repressor and activator of transcription and is specifically involved in the development of pancreatic beta cells, the thyroid, eye, liver and kidney. Mutations in this gene have been associated with neonatal diabetes and congenital hypothyroidism (NDH). Alternatively spliced variants that encode different protein isoforms have been described but the full-length nature of only two have been determined. [provided by RefSeq, Jul 2008] (from NCBI)
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Top mentioned proteins: Insulin, Gli, AGE, CAN, FADS1
Papers on GLIS3
Search for Rare Copy-Number Variants in Congenital Heart Defects Identifies Novel Candidate Genes and a Potential Role for FOXC1 in Patients with Coarctation of the Aorta.
Le Caignec et al., Nantes, France. In Circ Cardiovasc Genet, Jan 2016
We identified 113 candidate genes for CHD within these CNVs, including BTRC, CHRNB3, CSRP2BP, ERBB2, ERMARD, GLIS3, PLN, PTPRJ, RLN3 and TCTE3.
Association of type 2 diabetes GWAS loci and the risk of Parkinson's and Alzheimer's diseases.
Lee et al., Seoul, South Korea. In Parkinsonism Relat Disord, Dec 2015
We selected 32 genetic variants from 11 genes (CDC123, CDKAL1, CDKN2B, FTO, GLIS3, HHEX, IGF2BP2, KCNJ11, KCNQ1, SLC30A8, and TCF7L2) and intergenic regions based on results of recent genome-wide association studies (GWAS) in T2DM.
Expanding the Clinical Spectrum Associated With GLIS3 Mutations.
De Franco et al., Sheffield, United Kingdom. In J Clin Endocrinol Metab, Oct 2015
CONTEXT: GLIS3 (GLI-similar 3) is a member of the GLI-similar zinc finger protein family encoding for a nuclear protein with 5 C2H2-type zinc finger domains.
Heterogeneous phenotype in children affected by non-autoimmune hypothyroidism: an update.
Weber et al., Milano, Italy. In J Endocrinol Invest, Aug 2015
Finally, an increased prevalence of hypothyroidism has been documented in obese children and patients with syndromic forms (Williams, Down, Turner, pseudohypoparathyroidism). The clinical and molecular phenotype of patients with CH will be better defined thanks to novel genetic approach based on the systematic analysis of a panel of genes (TSHR, DUOX2, DUOXA, TPO, PDS, TG, NKX2.1, JAG1, GLIS3, FOXE1, PAX-8).
Statistical colocalization of genetic risk variants for related autoimmune diseases in the context of common controls.
Wallace et al., Cambridge, United Kingdom. In Nat Genet, Jul 2015
Four of eight T1D-specific regions contained known type 2 diabetes (T2D) candidate genes (COBL, GLIS3, RNLS and BCAR1), suggesting a shared cellular etiology.
Genetic link of type 1 diabetes susceptibility loci with rheumatoid arthritis in Pakistani patients.
Kamboh et al., Islamabad, Pakistan. In Immunogenetics, Jun 2015
We have identified seven SNP associations that survived multiple testing corrections using false discovery rate: SKAP2/rs7804356 (p = 2.47E-04), GLIS3/rs7020673 (p = 2.86E-04), GSDMB/rs2290400 (p = 23.48E-04),
HECT E3 Ubiquitin Ligase Itch Functions as a Novel Negative Regulator of Gli-Similar 3 (Glis3) Transcriptional Activity.
Jetten et al., United States. In Plos One, 2014
The transcription factor Gli-similar 3 (Glis3) plays a critical role in the generation of pancreatic ß cells and the regulation insulin gene transcription and has been implicated in the development of several pathologies, including type 1 and 2 diabetes and polycystic kidney disease.
Apoptosis of beta cells in diabetes mellitus.
Rani et al., Hyderābād, India. In Dna Cell Biol, 2014
The other gene products that are involved in diabetes are nitric oxide synthase-2 (NOS2), small ubiquitin-like modifier (SUMO), apolipoprotein CIII (ApoCIII), forkhead box protein O1 (FOXO1), and Kruppel-like zinc finger protein Gli-similar 3 (GLIS3).
Candidate genes for type 1 diabetes modulate pancreatic islet inflammation and β-cell apoptosis.
Eizirik et al., Brussels, Belgium. In Diabetes Obes Metab, 2013
Human β cell transcriptome analysis uncovers lncRNAs that are tissue-specific, dynamically regulated, and abnormally expressed in type 2 diabetes.
Ferrer et al., Barcelona, Spain. In Cell Metab, 2012
Depletion of HI-LNC25, a β cell-specific lncRNA, downregulated GLIS3 mRNA, thus exemplifying a gene regulatory function of islet lncRNAs.
Meta-analysis of genome-wide association studies identifies eight new loci for type 2 diabetes in east Asians.
Seielstad et al., South Korea. In Nat Genet, 2012
The combined analysis identified eight new T2D loci reaching genome-wide significance, which mapped in or near GLIS3, PEPD, FITM2-R3HDML-HNF4A, KCNK16, MAEA, GCC1-PAX4, PSMD6 and ZFAND3.
The Krüppel-like zinc finger protein GLIS3 transactivates neurogenin 3 for proper fetal pancreatic islet differentiation in mice.
Chan et al., Houston, United States. In Diabetologia, 2011
The results indicate that GLIS3 controls fetal islet differentiation via direct transactivation of Neurog3, a perturbation
Modulation of the transactivation function and stability of Krüppel-like zinc finger protein Gli-similar 3 (Glis3) by Suppressor of Fused.
Jetten et al., United States. In J Biol Chem, 2011
Glis3 interacts with Suppressor of Fused (SUFU)
Association of genetic Loci with glucose levels in childhood and adolescence: a meta-analysis of over 6,000 children.
Langenberg et al., Cambridge, United Kingdom. In Diabetes, 2011
Children and adolescents carrying glucose-raising alleles of G6PC2, MTNR1B, GCK, and GLIS3 also showed reduced beta-cell function, as indicated by homeostasis model assessment of beta-cell function.
Variants in GLIS3 and CRY2 are associated with type 2 diabetes and impaired fasting glucose in Chinese Hans.
Lin et al., Shanghai, China. In Plos One, 2010
the associations of GLIS3-rs7034200 and CRY2-rs11605924 with fasting glucose, beta cell function, and type 2 diabetes
Effects of 16 genetic variants on fasting glucose and type 2 diabetes in South Asians: ADCY5 and GLIS3 variants may predispose to type 2 diabetes.
Kelly et al., Birmingham, United Kingdom. In Plos One, 2010
Alleles of single nucleotide polymorphisms in GLIS3 and ADCY5 may confer risk of type 2 diabetes.
Gli-similar (Glis) Krüppel-like zinc finger proteins: insights into their physiological functions and critical roles in neonatal diabetes and cystic renal disease.
Jetten et al., United States. In Histol Histopathol, 2010
Mutations in human GLIS3 have been implicated in a syndrome characterized by neonatal diabetes and congenital hypothyroidism (NDH) and in some patients accompanied by polycystic kidney disease, glaucoma, and liver fibrosis.
New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.
Barroso et al., Boston, United States. In Nat Genet, 2010
These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1).
Genome-wide association study and meta-analysis find that over 40 loci affect risk of type 1 diabetes.
Type 1 Diabetes Genetics Consortium et al., Cambridge, United Kingdom. In Nat Genet, 2009
The many new candidate genes suggested by these results include IL10, IL19, IL20, GLIS3, CD69 and IL27.
Diagnosis of neonatal and infancy-onset diabetes.
Barbetti, Roma, Italy. In Endocr Dev, 2006
In about a decade, mutations in 8 different genes (IPF1, EIF2AK3, GK, FOXP3, KCNJ11, ABCC8, PTF1A and GLIS3) have been discovered in patients with the permanent form of the disease, and 3 genetic abnormalities (defects in the paternally imprinted chromosomal region 6q24 and 'mild' activating mutations in KCNJ11 or ABCC8) have been detected in subjects with transient neonatal diabetes.
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