2017
DOI: 10.1530/jme-16-0232
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Emerging roles of GLIS3 in neonatal diabetes, type 1 and type 2 diabetes

Abstract: GLI-similar 3 (GLIS3), a member of the Krüppel-like zinc finger protein subfamily, is predominantly expressed in the pancreas, thyroid and kidney. Glis3 mRNA can be initially detected in mouse pancreas at embryonic day 11.5 and is largely restricted to β cells, pancreatic polypeptide-expressing cells, as well as ductal cells at later stage of pancreas development. Mutations in GLIS3 cause a neonatal diabetes syndrome, characterized by neonatal diabetes, congenital hypothyroidism and polycystic kidney.

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Cited by 45 publications
(24 citation statements)
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References 75 publications
(105 reference statements)
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“…KLF4 is mainly engaged in the regulation of normal placentation and apoptosis (Blanchon et al 2001 ; Rowland et al 2005 ) while GLIS3 is implicated in the development of some fetal organs, such as the pancreas or thyroid (Dimitri 2017 ; Dimitri et al 2011 ; Nogueira et al 2013 ). Some case studies indicate that patients with a GLIS3 gene mutation resulting in a truncated non-functional protein demonstrated IUGR (Dimitri et al 2011 ).In addition, patients with disturbances in the GLIS3 gene demonstrate impaired beta cell function and an altered fasting glucose and diabetes mellitus phenotype (Wen and Yang 2017 ; Yang et al 2013 ). Further functional studies are needed to establish why the GLIS3 gene is depleted in the placentas of SGA (IUGR) fetuses developing in a limited energy environment.…”
Section: Discussionmentioning
confidence: 99%
“…KLF4 is mainly engaged in the regulation of normal placentation and apoptosis (Blanchon et al 2001 ; Rowland et al 2005 ) while GLIS3 is implicated in the development of some fetal organs, such as the pancreas or thyroid (Dimitri 2017 ; Dimitri et al 2011 ; Nogueira et al 2013 ). Some case studies indicate that patients with a GLIS3 gene mutation resulting in a truncated non-functional protein demonstrated IUGR (Dimitri et al 2011 ).In addition, patients with disturbances in the GLIS3 gene demonstrate impaired beta cell function and an altered fasting glucose and diabetes mellitus phenotype (Wen and Yang 2017 ; Yang et al 2013 ). Further functional studies are needed to establish why the GLIS3 gene is depleted in the placentas of SGA (IUGR) fetuses developing in a limited energy environment.…”
Section: Discussionmentioning
confidence: 99%
“…Another key molecule that could be linking thyroid and pancreas is transcription factor Gli-similar 3 (GLIS3). Variations of GLIS3 are strongly associated with both type 1 and type 2 diabetes in some populations [ 93 ]. GLIS3 can also coordinate with pancreatic and duodenal homeobox 1 (PDX1), MAFA, and neurogenic differentiation factor 1 (an insulin synthesis-related transcription factor) to potently regulate insulin gene transcription.…”
Section: Roles Of Thyroid and Thyroid Hormone In Pancreas Pathogenmentioning
confidence: 99%
“…GLIS3, a member of the Glis subfamily of Krüppel-like zinc-finger transcription factors, was characterized as modulating a set of essential cellular functions, such as insulin production, β-cell maintenance and maturation, stem and progenitor cell differentiation, and development. 40 , 41 Although studies converge on GLIS3 functioning in cancer, diabetes, hypothyroidism, and polycystic kidney disease, 40 , 42 , 43 , 44 the exact role of GLIS3 in human OA is unknown, and the miRNA regulating the expression of GLIS3 remains unclear. In this study, we demonstrated that GLIS3 was a direct target of miR-106a-5p.…”
Section: Discussionmentioning
confidence: 99%