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CDH13 locus variants and adiponectin (show ADIPOQ Proteins) 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.
The present study identified a new genetic factor for CRC (show CALR Proteins) risk and an interaction between CDH13 and APN (show ANPEP Proteins) in CRC (show CALR Proteins) risk. These genetic factors may be useful for predicting CRC (show CALR Proteins) risk.
The downregulation of T-cadherin may contribute to gastric cancer progression, representing a useful biomarker for predicting the biological behavior and prognosis of gastric cancer.
Finnish prisoners, revealed that a monoamine oxidase A (MAOA (show MAOA Proteins)) low-activity genotype (contributing to low dopamine turnover rate) as well as the CDH13 gene (coding for neuronal membrane adhesion protein) are associated with extremely violent behavior
The genetic polymorphisms at the CDH13 locus independently affect the adiponectin (show ADIPOQ Proteins) levels, whereas the adiponectin (show ADIPOQ Proteins) levels exhibit a suppressive effect on the association between CDH13 locus variants and various metabolic phenotypes and metabolic syndrome
The CDH13 rs11150556 CC genotype was associated with more hyperactive/impulsive symptoms in attention/deficit hyperactivity disorder.
CDH13 promoter methylation is associated with lung cancer.
Aberrant promoter methylation of the cadherin 13 gene in serum is associated with prostate cancer.
Our results suggested that negative T-cadherin expression has a worse prognosis in patients with axillary lymph node-positive breast cancer.
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 (show ADIPOQ Proteins).
T-cad does not mediate the protective effects of adiponectin (show ADIPOQ Proteins) in allergic airways responses in mice
T-cadherin is a component of insulin (show INS Proteins) granules, suggesting that it contributes to the regulation of insulin (show INS Proteins) secretion independently of direct interactions with adiponectin (show ADIPOQ Proteins).
T-cad can exert pleiotropic effects on squamous cell carcinoma progression; up- or down-regulation of T-cad can promote tumour expansion in vivo.
T-cadherin protects from stress-induced pathological cardiac remodeling by binding APN (show ANPEP Proteins) and activating its cardioprotective functions.
hyperexpression of T-cadherin in the B16F10 cells suppresses the proliferation of these cells in vitro and the growth of the tumor masses formed by melanoma cells on the chorioallantoic membrane and their neovascularization
Expression of T-cadherin in Basal keratinocytes of skin.
T-cadherin has a role in growth regulation involving p21(CIP1/WAF1 (show CDKN1A Proteins)) expression and G2 arrest
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