Search Within
SML2702
Keyword:'SML2702'
Showing 1-12 of 12 results for "SML2702" within Papers
Biochemical and biophysical research communications, 478(4), 1497-1502 (2016-08-18)
GNB2L1 is an intercellular scaffold protein of the Trp-Asp (WD) repeat protein family, and has been reported to play suppressive roles in the progression of gastric cancer. However, the regulatory mechanisms of GNB2L1 in gastric cancer still remain largely elusive.
Microbes and infection, 20(6), 376-384 (2018-06-04)
Trichomonas vaginalis is a sexually-transmitted protozoan parasite that causes vaginitis and cervicitis. Although mast cell activation is important for provoking tissue inflammation during infection with parasites, information regarding the signaling mechanisms in mast cell activation and T. vaginalis infection is
The Journal of biological chemistry, 288(47), 33927-33938 (2013-10-17)
Pancreatic cancer, the fourth most prevalent cancer-related cause of death in the United States, is a disease with a dismal survival rate of 5% 5 years after diagnosis. One of the survival proteins responsible for its extraordinary ability to evade
Cell reports, 24(8), 1931-1938 (2018-08-23)
Regrowth of an axon after injury is an inherently metabolic undertaking. Yet the mechanisms of metabolic regulation that influence repair following injury are not well understood. O-linked β-N-acetylglucosamine (O-GlcNAc) is a post-translational modification of serines and threonines that functions as
Cell death & disease, 9(10), 970-970 (2018-09-22)
Rab3A is a small Ras-like GTPase critical for membrane traffic. Although the functions of Rab3A have been reported in several cancers, the roles of Rab3A in hepatocellular carcinoma (HCC) have never been determined. To investigate the potential roles of Rab3A
Cardiovascular research, 107(2), 295-306 (2015-06-04)
We hypothesized that a disproportionate activation of the glucosamine (GlcN) pathway, caused by a prolonged exposure to hyperglycaemia, could impair endothelial integrity promoting endoplasmic reticulum (ER) stress. We also tested the possibility that SRT1720 may be able to counteract GlcN-induced
Cellular signalling, 28(5), 384-390 (2016-02-09)
Resistance to insulin action is a key cause of diabetic complications, yet much remains unknown about the molecular mechanisms that contribute to the defect. Glucose-induced insulin resistance in peripheral tissues such as the retina is mediated in part by the
The lineage stability and suppressive program of regulatory T cells require protein O-GlcNAcylation.
Nature communications, 10(1), 354-354 (2019-01-22)
Regulatory T (Treg) cells control self-tolerance, inflammatory responses and tissue homeostasis. In mature Treg cells, continued expression of FOXP3 maintains lineage identity, while T cell receptor (TCR) signaling and interleukin-2 (IL-2)/STAT5 activation support the suppressive effector function of Treg cells
Virology, 531, 183-191 (2019-03-31)
Human metapneumovirus (hMPV) is an important cause of acute lower respiratory tract infections in infants, elderly and immunocompromised individuals. Ingenuity pathway analysis of microarrays data showed that 20% of genes affected by hMPV infection of airway epithelial cells (AECs) were
Journal of the American Chemical Society, 127(42), 14588-14589 (2005-10-20)
O-GlcNAcylation of serine and threonine residues is a dynamic and essential post-translational modification involved in signaling pathways in eukaryotes. Studies of O-GlcNAcylation would be aided by small-molecule inhibitors of O-GlcNAc transferase (OGT), the sole enzyme know to mediate this modification
Scientific reports, 7(1), 11107-11107 (2017-09-13)
Diabetes mellitus in early pregnancy can cause neural tube defects (NTDs) in embryos by perturbing protein activity, causing cellular stress, and increasing programmed cell death (apoptosis) in the tissues required for neurulation. Hyperglycemia augments a branch pathway in glycolysis, the
The Journal of clinical investigation, 128(11), 4924-4937 (2018-08-22)
Mutant KRAS drives glycolytic flux in lung cancer, potentially impacting aberrant protein glycosylation. Recent evidence suggests aberrant KRAS drives flux of glucose into the hexosamine biosynthetic pathway (HBP). HBP is required for various glycosylation processes, such as protein N- or
Page 1 of 1