Anti-Human CADM2 Antibody (CPBT-51829RH)

Rabbit anti-Human CADM2 Polyclonal antibody for ICC/IF, WB, ELISA

Specifications


Host Species
Rabbit
Antibody Isotype
IgG
Species Reactivity
Human
Immunogen
Synthetic peptide (Human)
Conjugate
Unconjugated

Target


Alternative Names
CADM2; cell adhesion molecule 2; IGSF4D,immunoglobulin superfamily, member 4D; Necl 3; NECL3; nectin like 3
Entrez Gene ID
UniProt ID

Product Background


Gene summary
CADM2 (Cell Adhesion Molecule 2) is a Protein Coding gene. Among its related pathways are Cell junction organization. An important paralog of this gene is CADM3. This gene encodes a member of the synaptic cell adhesion molecule 1 (SynCAM) family which belongs to the immunoglobulin (Ig) superfamily. The encoded protein has three Ig-like domains and a cytosolic protein 4. 1 binding site near the C-terminus. Proteins belonging to the protein 4. 1 family crosslink spectrin and interact with other cytoskeletal proteins. Multiple transcript variants encoding different isoforms have been found for this gene.
Antigen Description
Members of the large immunoglobulin (Ig) superfamily, such as IGSF4D, have diverse roles in extracellular recognition and intercellular adhesion (Biederer, 2006Adhesion molecule that engages in homo- and heterophilic interactions with the other nectin-like family members, leading to cell aggregation. Important for synapse organization, providing regulated trans-synaptic adhesion. Preferentially binds to oligodendrocytes.
Pathway
Adherens junctions interactions, organism-specific biosystem; Cell junction organization, organism-specific biosystem; Cell-Cell communication, organism-specific biosystem; Cell-cell junction organization, organism-specific biosystem.

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We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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References


Robust analysis of novel mRNA-IncRNA cross talk based on ceRNA hypothesis uncovers carcinogenic mechanism and promotes diagnostic accuracy in esophageal cancer

CANCER MANAGEMENT AND RESEARCH

Authors: Chen, Li-Ping; Wang, Hong; Zhang, Yi; Chen, Qiu-Xiang; Lin, Tie-Su; Liu, Zong-Qin; Zhou, Yang-Yang

Background: ceRNAs have emerged as pivotal players in the regulation of gene expression and play a crucial role in the physiology and development of various cancers. Nevertheless, the function and underlying mechanisms of ceRNAs in esophageal cancer (EC) are still largely unknown. Methods: In this study, profiles of DEmRNAs, DEIncRNAs, and DEmiRNAs between normal and EC tumor tissue samples were obtained from the Cancer Genome Atlas database using the DESeq package in R by setting the adjusted P<0.05 and |log(2) (fold change)|>2 as the cutoff The ceRNA network (ceRNet) was initially constructed to reveal the interaction of these ceRNAs during carcinogenesis based on the bioinformatics of miRcode, miRDB, miRTarBase, and TargetScan. Then, independent microarray data of GSE6188, GSE89102, and GSE92396 and correlation analysis were used to validate molecular biomarkers in the initial ceRNet. Finally, a least absolute shrinkage and selection operator logistic regression model was built using an oncogenic ceRNet to diagnose EC more accurately. Results: We successfully constructed an oncogenic ceRNet of EC, crosstalk of hsa-miR372-centered CADM2-ADAMTS9-AS2 and hsa-miR145-centered SERPINE1-PVT1. In addition, the risk-score model -0.0053*log(2)(CADM2)+0.0168*log(2)(SERPINE/)-0.0073*log(2)(ADAMTS9-AS2)+0.0905*log(2)(PVT1)+0.0047*log(2)(hsa-miR372)-0.0193*log(2)(hsa-miR145), (log(2)[gene count]) could improve diagnosis of EC with an AUC of 0.988. Conclusion: We identified two novel pairs of ceRNAs in EC and its role of diagnosis. The pairs of hsa-miR372-centered CADM2-ADAMTS9-AS2 and hsa-miR145-centered SERPINE1-PVT1 were likely potential carcinogenic mechanisms of EC, and their joint detection could improve diagnostic accuracy.

MicroRNA-125a-3p is involved in early behavioral disorders in stroke-afflicted rats through the regulation of Cadm2

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE

Authors: Liu, Yuqing; Li, Yunjun; Ren, Zhenxing; Si, Wenwen; Li, Yiwei; Wei, Gang; Zhao, Wenguang; Zhou, Jianhong; Tian, Yage; Chen, Dongfeng

Ischemic strokes carry a significant risk of mortality and recurrent vascular events. Recent studies suggest that changes in microRNAs (miRNAs or miRs) may affect the development of the stroke. However, few studies have investigated the role of miRNAs in behavioral disorder in early stroke. In the present study, animal models of middle cerebral artery occlusion (MCAO) are used, as well as a cell model of neurite outgrowth to further investigate the role of miRNAs in targeting synapse-associated proteins expression in early stroke. The authors used miRNA expression microarrays on RNA extracted from the cortex tissue samples from the rats of MCAO and control rats. Reverse transcription-quantitative polymerase chain reaction was conducted to verify the candidate miRNAs discovered by microarray analysis. Data indicated that miR-125a was significantly increased in the cortex of the model of MCAO, which were concomitant with that rats of MCAO at the same age displayed significant behavioral deficits. Bioinformatics analysis predicted the cell adhesion molecule 2 (Cadm2, mRNA) neurite outgrowth-associated protein is targeted by miR-125a. Overexpression of miR-125a reduced the level of Cadm2 expression in PC12 cell injury induced by free-serum. In contrast, inhibition of miR-125a using miR-125a inhibitors significantly resulted in higher levels of Cadm2 expression. In conclusion, miR-125a is involved in the behavioral disorder of animal models of MCAO by regulation of Cadm2.

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