Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
The CTX (see VSIG2, MIM 606011) family of proteins, including ASAM, are type I transmembrane proteins within the Ig superfamily that localize to junctional complexes between endothelial and epithelial cells and may play a role in cell-cell adhesion (Raschperger et al., 2004 [PubMed 14573622]).[supplied by OMIM, Mar 2008].. De plus, nous expédions CLMP Protéines (20) et CLMP Kits (13) et beaucoup plus de produits pour cette protéine.
Showing 10 out of 74 products:
Human Polyclonal CLMP Primary Antibody pour ELISA, WB - ABIN4281764
Raschperger, Engstrom, Pettersson, Fuxe: CLMP, a novel member of the CTX family and a new component of epithelial tight junctions. dans The Journal of biological chemistry 2003
We describe a newborn presenting CSBS intestinal malrotation and chronic intestinal pseudo-obstruction syndrome (CIPS), compound heterozygous for two previously unreported heterozygous mutations in Coxsackie and adenovirus receptor-like membrane protein (CLMP) gene. We identified two heterozygous mutations in CLMP, one in intron 1 (c.28+1G>C) from the father, the other on exon 4 (c502C>T, p.R168X) from the mother.
Inhibition of CFTR or histone deacetylase (HDAC) enhanced CAR expression while CFTR overexpression or restoration of the diminished HDAC activity in cystic fibrosis cells reduced CAR expression.
Novel inherited variants in CLMP were identified in three congenital short bowel syndrome patients derived from two unrelated families.
The key processes involved in intestinal epithelial development appear to be unaffected by wild type-CLMP or mutant-CLMP.
Coxsackievirus and adenovirus receptor gene expression is induced in esophageal cancer cells by the HDAC inhibitor trichostatin A.
The PDZ1 and PDZ3 domains of MAGI-1 regulate the eight-exon isoform of the CXADR-like membrane protein.
Loss-of-function mutations in CLMP cause congenital short bowel syndrome in human beings, likely by interfering with tight-junction formation, which disrupts intestinal development.
CLMP is a novel cell-cell adhesion molecule and a new component of epithelial tight junctions.
We identified ACAM (adipocyte adhesion molecule), a novel homologue of the CTX (cortical thymocyte marker in Xenopus) gene family, which may be the critical adhesion molecule in adipocyte differentiation and development of obesity.
ASAM, IGSF11, CXADR and ESAM are type I transmembrane proteins and members of the same IGSF superfamily.
the levels of mRNAs encoding Connexin43 or Connexin45 were not or were only marginally affected, respectively, by Clmp deficiency, the absence of CLMP caused a severe reduction of both proteins in smooth muscle cells of the intestine and of Connexin43 in the ureter.
Data (including data from studies in transgenic mice) suggest that, when Acam/Clmp is abundantly expressed on plasma membrane of mature adipocytes, mice are protected from obesity and diabetes with prominent reduction of adipose tissue mass and smaller size of adipocytes; studies used high-fat, high-sucrose diet to induce obesity and diabetes in control mice.
Expression of CLMP, a novel tight junction protein, is mediated via the interaction of GATA with the Kruppel family proteins, KLF4 and Sp1, in mouse TM4 Sertoli cells.
TNFalpha-mediated mRNA degradation of the CLMP gene is controlled by TTP through the JNK signalling cascade
The CTX (see VSIG2, MIM 606011) family of proteins, including ASAM, are type I transmembrane proteins within the Ig superfamily that localize to junctional complexes between endothelial and epithelial cells and may play a role in cell-cell adhesion (Raschperger et al., 2004
CAR-like membrane protein
, adipocyte adhesion molecule
, adipocyte-specific adhesion molecule
, coxsackie- and adenovirus receptor-like membrane protein
, visceral adipose tissue-specific transmembrane protein OL-16
, adipocyte-specific protein 5