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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].. Zusätzlich bieten wir Ihnen CLMP Antikörper (69) und CLMP Proteine (18) und viele weitere Produktgruppen zu diesem Protein an.
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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 (zeige CFTR ELISA Kits) or histone deacetylase (HDAC (zeige HDAC1 ELISA Kits)) enhanced CAR expression while CFTR (zeige CFTR ELISA Kits) overexpression or restoration of the diminished HDAC (zeige HDAC3 ELISA Kits) activity in cystic fibrosis (zeige S100A8 ELISA Kits) 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 (zeige CXADR ELISA Kits) gene expression is induced in esophageal cancer cells by the HDAC (zeige HDAC3 ELISA Kits) inhibitor trichostatin A.
The PDZ1 and PDZ3 domains of MAGI-1 (zeige MAGI1 ELISA Kits) 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 (zeige PCDHB16 ELISA Kits) 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 (zeige IGSF11 ELISA Kits), CXADR (zeige CXADR ELISA Kits) and ESAM (zeige ESAM ELISA Kits) are type I transmembrane proteins and members of the same IGSF superfamily.
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 (zeige OCLN ELISA Kits), is mediated via the interaction of GATA (zeige QRSL1 ELISA Kits) with the Kruppel family proteins, KLF4 (zeige KLF4 ELISA Kits) and Sp1 (zeige SP1 ELISA Kits), in mouse TM4 (zeige TPM4 ELISA Kits) Sertoli cells.
TNFalpha (zeige TNF ELISA Kits)-mediated mRNA degradation of the CLMP gene is controlled by TTP (zeige ZFP36 ELISA Kits) through the JNK (zeige MAPK8 ELISA Kits) 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