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ITM2C Monoclonal antibody, PBS Only

ITM2C Monoclonal Antibody for IF/ICC, Indirect ELISA

Host / Isotype

Mouse / IgG2a

Reactivity

human

Applications

IF/ICC, Indirect ELISA

Conjugate

Unconjugated

CloneNo.

2E8G11

Cat no : 60095-1-PBS

Synonyms

BRICD2C, Cerebral protein 14, E25, E25C, integral membrane protein 2C, ITM2C, ITM3, PSEC0047, Transmembrane protein BRI3

Validation Data Gallery

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  • Immunofluorescence (IF) / fluorescent staining of HepG2 cells using ITM2C Monoclonal antibody (60095-1-Ig)

    IF Staining of HepG2 using 60095-1-Ig (same clone as 60095-1-PBS)

    Immunofluorescent analysis of HepG2 cells using 60095-1-Ig (ITM2C antibody) at dilution of 1:50 and Rhodamine-Goat anti-Mouse IgG. This data was developed using the same antibody clone with 60095-1-PBS in a different storage buffer formulation.

Product Information

60095-1-PBS targets ITM2C in IF/ICC, Indirect ELISA applications and shows reactivity with human samples.

Tested Reactivity human
Host / Isotype Mouse / IgG2a
Class Monoclonal
Type Antibody
Immunogen ITM2C fusion protein Ag4409
Full Name integral membrane protein 2C
Calculated Molecular Weight230aa,26 kDa; 267aa,30 kDa
Observed Molecular Weight 35 kDa
GenBank Accession NumberBC025742
Gene Symbol ITM2C
Gene ID (NCBI) 81618
Conjugate Unconjugated
Form Liquid
Purification MethodProtein A purification
Storage Buffer PBS Only
Storage ConditionsStore at -80°C.

Background Information

The Integral membrane protein 2C (ITM2C) is a type II integral transmembrane protein belonging to a family composed of at least two other members, ITM2A and ITM2B. ITM2C, often called transmembrane protein BRI3, is highly expressed in brain tissue. Yeast two-hybrid screen system revealed that BRI3 could interact with beta-secretase beta-amyloid protein converting enzyme (BACE)1 and the microtubule-destabilizing protein SCG10 (STMN2). It may play a role in TNF-induced cell death and neuronal differentiation. BRI3 was found to inhibit the various processing of amyloid precursor protein (APP) by blocking the access of alpha- and beta-secretases to APP, competitive inhibition of APP processing by BRI3 may provide a new approach to Alzheimer disease (AD) therapy and prevention.