Results 11 to 20 of about 13,098 (176)

Underestimated risk of secondary complications in pathogenic and glucose-elevating GCK variant carriers with type 2 diabetes

open access: yesCommunications Medicine
Background Natural HbA1c levels in GCK Maturity-onset diabetes of the young (GCK-MODY) patients often sit above the diagnostic threshold for type 2 diabetes (T2D).
Kelly M. Schiabor Barrett   +10 more
doaj   +2 more sources

Genetic and clinical characteristics of Chinese children with Glucokinase-maturity-onset diabetes of the young (GCK-MODY) [PDF]

open access: yesBMC Pediatrics, 2018
Background There is scarcity of information on the clinical features and genetics of glucokinase-maturity-onset diabetes of the young (GCK-MODY) in China.
Xiuzhen Li   +8 more
doaj   +2 more sources

Identification of pathogenic GCK variants in patients with common type 2 diabetes can lead to discontinuation of pharmacological treatment [PDF]

open access: yesMolecular Genetics and Metabolism Reports, 2023
Background: Functionally disruptive variants in the glucokinase gene (GCK) cause a form of mild non-progressive hyperglycemia, which does not require pharmacological treatment.
Anne Cathrine Baun Thuesen   +14 more
doaj   +2 more sources

The germinal center kinase GCK-1 is a negative regulator of MAP kinase activation and apoptosis in the C. elegans germline. [PDF]

open access: yesPLoS ONE, 2009
The germinal center kinases (GCK) constitute a large, highly conserved family of proteins that has been implicated in a wide variety of cellular processes including cell growth and proliferation, polarity, migration, and stress responses.
Katherine R Schouest   +5 more
doaj   +2 more sources

Chronic Mild Hyperglycemia in GCK-MODY Patients Does Not Increase Carotid Intima-Media Thickness [PDF]

open access: yesInternational Journal of Endocrinology, 2013
Aim. GCK-MODY is an autosomal dominant form of diabetes caused by heterozygous mutations in the glucokinase gene leading to a lifelong mild hyperglycemia. The risk of macrovascular complications is considered low, but studies are limited.
Stepanka Pruhova   +11 more
doaj   +2 more sources

Molecular genetic analysis and clinical consideration of two families with GCK gene mutation [PDF]

open access: yesJichu yixue yu linchuang, 2020
Objective To explore the molecular genetics and clinical characteristics of two cases of maturity-onset diabetes of the young (MODY) type 2 caused by glucokinase (GCK) gene mutation.
WANG Zhi-xin, ZUO Qing-yao, LI Wei, CHEN Jia, DENG Wei
doaj   +1 more source

Intestinal peroxisome proliferator‐activated receptor α‐fatty acid‐binding protein 1 axis modulates nonalcoholic steatohepatitis

open access: yesHepatology, EarlyView., 2022
Abstract Background and Aims Peroxisome proliferator‐activated receptor α (PPARα) regulates fatty acid transport and catabolism in liver. However, the role of intestinal PPARα in lipid homeostasis is largely unknown. Here, intestinal PPARα was examined for its modulation of obesity and NASH. Approach and Results Intestinal PPARα was activated and fatty
Tingting Yan   +22 more
wiley   +1 more source

DataSheet1_GCK exonic mutations induce abnormal biochemical activities and result in GCK-MODY.docx

open access: yes, 2023
Objective: Glucokinase-maturity-onset diabetes of the young (GCK-MODY; MODY2) is a rare genetic disorder caused by mutations in the glucokinase (GCK) gene.
Lifen Chen (3769015)   +14 more
core   +1 more source

Capping Protein Interacts with GCK-1 and CCM-3 during C. elegans Zygote Cytokinesis [PDF]

open access: yes, 2022
During cytokinesis, the remodeling of the actomyosin contractile ring separates a single cell into two daughter cells. The equatorial ring undergoes cortical remodeling and contraction, and the physical splitting of a single cell accurately partitions ...
Wan, Zixuan
core   +1 more source

Glucokinase links Kruppel-like factor 6 to the regulation of hepatic insulin sensitivity in nonalcoholic fatty liver disease [PDF]

open access: yes, 2011
The polymorphism, KLF6-IVS1-27A, in the Krüppel-like factor 6 (KLF6) transcription factor gene enhances its splicing into antagonistic isoforms and is associated with delayed histological progression of nonalcoholic fatty liver disease (NAFLD).
Gastaldelli, Amalia   +103 more
core   +1 more source

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