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CDH13 genetic polymorphisms are associated with adiponectin levels and ischemic stroke.
Study evaluated the associations between 6 SNPs in CDH13 and type 2 diabetes mellitus (T2DM) in a Han Chinese population. Results showed that the rs12596316 AG genotype was a risk genotype for the development of T2DM in the overdominant inheritance model; rs11646213, rs3865188, rs12444338, rs12051272, and rs7195409 had no observed associations with T2DM in terms of alleles, genotypes, and the various inheritance models.
The methylation status of CDH13 promoter was strongly associated with breast cancer risk. However, CDH13 promoter methylation was not significantly related to the OS and DFS (show FST Proteins) of breast cancer and may have limited prognostic value for breast cancer patients
Studied the associations between genetic variants of CDH13 and type 2 diabetes (T2D), and its related parameters, in a Caucasian population.
Compared with adjacent normal tissues, the methylation frequencies of WIF-1 (show WIF1 Proteins), RASSF1A (show RASSF1 Proteins), and CDH13 genes were significantly higher but the mRNA levels of these 3 genes were significantly lower in EC tissues. The survival rates of patients with WIF-1 (show WIF1 Proteins), RASSF1A (show RASSF1 Proteins), and CDH13 methylations were significantly lower than those of patients without methylation
CDH13 genetic variants determine Chinese individuals' susceptibility to chronic obstructive pulmonary disease (COPD (show ARCN1 Proteins)) and thus are efficient genetic biomarkers for early detection of COPD (show ARCN1 Proteins).
Strong Functional Association of adipor2 and cdh13 with adipoq
CDH13 Polymorphisms are Associated with Adiponectin Levels and Metabolic Syndrome Traits Independently of Visceral Fat Mass.
CDH13 locus variants and adiponectin levels are associated with circulating levels of cellular adhesion molecules and adiposity status in a differential manner that interacts with sex
Data demonstrate for the first time that SHP1 (show PTPN6 Proteins) methylation has high specificity for diagnosis of endometrial carcinoma, while CDH13 promoter methylation plays a role in the earlier stage.
using rat and murine aortic smooth muscle cells as experimental models, we surveyed the ability of T-cadherin to regulate autophagy in SMCs during serum-starvation stress. Overall our findings have identified T-cadherin as a novel positive regulator of autophagy and survival in smooth muscle cells
T-cadherin was essential for accumulation of adiponectin in the neointima and atherosclerotic plaque lesions, and the adiponectin-T-cadherin association protected against vascular injury.
T-cadherin deficiency causes endothelial dysfunction in Type II Diabetes Mellitus.
a unique key feature of the T-cad prodomain is its involvement in binding of the T-cad repeats 1 and 2 to adiponectin; adiponectin positively regulates T-cad abundance
CDH13 is a negative regulator of inhibitory synapses in the hippocampus, and provide insights into how CDH13 dysfunction may contribute to the excitatory/inhibitory imbalance observed in Attention Deficit Disorder with Hyperactivity.
These data show that both circulating and tissue-bound Adipo levels are dependent on Tcad and, in reverse, regulate tissue Tcad levels through a positive feedback loop.
These data highlight a previously unrecognized role for T-cadherin in limb revascularization and show that it is essential for mediating the vascular actions of adiponectin.
T-cad does not mediate the protective effects of adiponectin in allergic airways responses in mice
T-cadherin is a component of insulin granules, suggesting that it contributes to the regulation of insulin secretion independently of direct interactions with adiponectin.
T-cad can exert pleiotropic effects on squamous cell carcinoma progression; up- or down-regulation of T-cad can promote tumour expansion in vivo.
This gene encodes a member of the cadherin superfamily. The encoded protein is localized to the surface of the cell membrane and is anchored by a GPI moiety, rather than by a transmembrane domain. The protein lacks the cytoplasmic domain characteristic of other cadherins, and so is not thought to be a cell-cell adhesion glycoprotein. This protein acts as a negative regulator of axon growth during neural differentiation. It also protects vascular endothelial cells from apoptosis due to oxidative stress, and is associated with resistance to atherosclerosis. The gene is hypermethylated in many types of cancer. Alternative splicing results in multiple transcript variants encoding different isoforms.
, H-cadherin (heart)
, cadherin 13, H-cadherin (heart)
, heart cadherin