Anti-CLEC2A Antibody

C-type lectin domain family 2 member A (CLEC2A) is also called proliferation-induced lymphocyte-associated receptor (PILAR) and Keratinocyte-associated C-type lectin (KACL). CLEC2A is involved in modulating T-cell expansion. It is a 32 kDa single-pass type II membrane protein that belongs to the CTL/CTLD superfamily. CLEC2A is mainly expressed in skin and highly expressed in CD8(+), B lymphocytes and naive CD4(+) T cells. Modulation of CLEC2A signaling may be important for treatment of autoimmune diseases and cancer. CLEC2A is associated with expansion of TCR-stimulated T-cells, modulates the capacity of T-cells to home to lymph nodes through SELL, and facilitates immune recognition of keratinocytes by stimulating natural killer cell mediated cytotoxicity.

~32 kDa observed. Uncharacterized bands may appear in some lysate(s). Uniprot describes 2 isoforms at ~19 kDa and ~20 kDa

KLH-conjugated linear peptide corresponding to human CLEC2A.

Anti-CLEC2A Antibody is a highly specific rabbit polyclonal antibody, that targets CLEC2A & has been tested in western blotting.

Research Category
Apoptosis & Cancer

Research Sub Category
Apoptosis - Additional

Antigen Affinity Purified

Purified rabbit polyclonal in buffer containing PBS with up to 0.1% sodium azide.

Stable for 1 year at 2-8°C from date of receipt.

Control
K562 cell lysate

Evaluated by Western Blotting/Peptide Inhibition Assay in K562 cell lysate.

Western Blotting/Peptide Inhibition Analysis: 1 µg/mL of this antibody detected CLEC2A in 15 µg of K562 cell lysate.

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.