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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 GLIS Family Zinc Finger 3 Antibodies (11) and and many more products for this protein.
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 ELISA Kits)-PRKCA (show PKCa ELISA Kits) and CLPTM1L (show CLPTM1L ELISA Kits)-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 ELISA Kits) may confer risk of type 2 diabetes.
the associations of GLIS3-rs7034200 and CRY2 (show CRY2 ELISA Kits)-rs11605924 with fasting glucose, beta cell function, and type 2 diabetes
Glis3 interacts with Suppressor of Fused (SUFU (show SUFUH ELISA Kits))
Children and adolescents carrying glucose-raising alleles of G6PC2, MTNR1B (show MTNR1B ELISA Kits), GCK (show GCK ELISA Kits), and GLIS3 also showed reduced beta-cell function, as indicated by homeostasis model assessment of beta-cell function.
results demonstrate a major role for GLIS3 in the development of pancreatic beta cells and the thyroid, eye, liver and kidney
Glis3 plays a pivotal role in the transcriptional regulation of insulin (show INS ELISA Kits).
beta cell-specific inactivation of Glis3 in adult mice downregulates insulin (show INS ELISA Kits) 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 ELISA Kits), 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 ELISA Kits) 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 ELISA Kits) mRNA level in the pancreas caused by impaired islet development and the subsequent impairment of Insulin (show INS ELISA Kits)-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 ELISA Kits) 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.
GLIS family zinc finger 3
, zinc finger protein GLIS3
, GLI-similar 3
, zinc finger protein 515
, Kruppel-like zinc finger protein Glis3