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GLIS3 is a member of the GLI-similar zinc finger protein family and encodes a nuclear protein with five C2H2-type zinc finger domains. Additionally we are shipping and many more products for this protein.
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we describe the common facial dysmorphism consisting of bilateral low-set ears, depressed nasal bridge with overhanging columella, elongated, upslanted palpebral fissures, persistent long philtrum with a thin vermilion border of the upper lip in a cohort of seven patients with GLIS3 mutations and report the emergence of a distinct, probably recognizable facial gestalt in this group which evolves with age.
It may play a role in a number of physiological processes controlled by Glis3.
New findings with GLIS3 phenotype including craniosynostosis, hiatus hernia, atrial septal defect, splenic cyst, and choanal atresia and confirm further cases with sensorineural deafness and exocrine pancreatic insufficiency.
Whole exome sequencing followed by immunohistochemistry of fibrolamellar hepatocellular carcinoma cell lines and tumors showed two structural variants resulting in fusion transcripts: DNAJB1 (show DNAJB1 Antibodies)-PRKCA (show PKCa Antibodies) and CLPTM1L (show CLPTM1L Antibodies)-GLIS3.
analysis of a GLIS3 variant that may have a role in resistance to Japanese type 1 diabetes
The present data suggest that altered expression of the candidate gene GLIS3 may contribute to both type 1 and 2 type diabetes by favouring beta cell apoptosis
Alleles of single nucleotide polymorphisms in GLIS3 and ADCY5 (show ADCY5 Antibodies) may confer risk of type 2 diabetes.
the associations of GLIS3-rs7034200 and CRY2 (show CRY2 Antibodies)-rs11605924 with fasting glucose, beta cell function, and type 2 diabetes
Glis3 interacts with Suppressor of Fused (SUFU (show SUFUH Antibodies))
Children and adolescents carrying glucose-raising alleles of G6PC2, MTNR1B (show MTNR1B Antibodies), GCK (show GCK Antibodies), and GLIS3 also showed reduced beta-cell function, as indicated by homeostasis model assessment of beta-cell function.
Study demonstrates that Glis3 protein exhibits a temporal and cell type-specific pattern of expression during embryonic and neonatal pancreas development that is consistent with a regulatory role for Glis3 in promoting endocrine progenitor generation, regulating insulin (show INS Antibodies) and Ppy (show PPY Antibodies) expression in beta and Ppy (show PPY Antibodies) expression in beta and PP cells, respectively, and duct morphogenesis.
Glis3 plays a pivotal role in the transcriptional regulation of insulin (show INS Antibodies).
beta cell-specific inactivation of Glis3 in adult mice downregulates insulin (show INS Antibodies) expression, leading to hyperglycaemia and subsequently enhanced beta cell apoptosis
The results indicate that GLIS3 controls fetal islet differentiation via direct transactivation of Neurog3 (show NEUROG3 Antibodies), a perturbation
The transcription factor, GLIS3, has both repressor and activation functions.
Data show that dysfunction of Glis3 leads to the development of cystic renal disease, and suggest that localization to the primary cilium and interaction with Wwtr1 (show WWTR1 Antibodies) are key elements of the Glis3 signaling pathway.
Glis3(-/-) mice had increases in the blood sugar level in the first days after birth, attributed to a decrease in Insulin (show INS Antibodies) mRNA level in the pancreas caused by impaired islet development and the subsequent impairment of Insulin (show INS Antibodies)-producing cell formation.
Data show that Glis3 plays a role in cell lineage specification, particularly in the development of pancreatic beta cells, and also regulates insulin (show INS Antibodies) gene expression.
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.
, zinc finger protein 515
, zinc finger protein GLIS3
, Kruppel-like zinc finger protein Glis3
, GLIS family zinc finger 3