Anti-Human CD152 (CTLA-4) Purified

Also known as: CTLA4

Clone: 14D3

RUO: For Research Use Only. Not for use in diagnostic procedures.

SKU# 14-1529

Cat. No. Size
14-1529-80 25 ug
14-1529-82 100 ug
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Data for Anti-Human CD152 (CTLA-4) Purified.

Description

Description: The 14D3 monoclonal antibody reacts with human CD152, also known as cytotoxic T lymphocyte antigen-4 (CTLA-4). CTLA-4, a protein with structural similarities to CD28, is expressed on activated T cells (activated B cells may also express CTLA-4) and binds the B7 family members, CD80 (B7-1) and CD86 (B7-2), with higher affinity than CD28 does. CTLA-4 and CD28 appear to deliver opposing signals to T cells: while CD28 is a potent costimulator, CTLA-4 restricts the progression of T cells to an activated state by inhibiting IL-2 secretion and cellular proliferation. The cytoplasmic portion of CTLA-4 contains ER retention motifs, resulting in intracellular localization of a large proportion of newly synthesized CTLA-4 in response to TCR signaling.

Details
Host Mouse
Isotype IgG2a
Reactivity Human
Conjugate Purified
Reported Applications Flow Cytometric Analysis, Immunohistochemical Staining of Frozen Tissue Sections, Functional Assays
Documentation

For complete product information, please download the TDS or IFU document.

TDS Link Download TDS
Additional Formats
Cat. No. Name Excite Emit Application Reg.
13-1529 Anti-Human CD152 (CTLA-4) Biotin FC RUO
12-1529 Anti-Human CD152 (CTLA-4) PE 488 - 561 nm 575 nm FC RUO
16-1529 Anti-Human CD152 (CTLA-4) Functional Grade Purified FC, FA RUO
References

References: Saverino D, Brizzolara R, Simone R, Chiappori A, Milintenda-Floriani F, Pesce G, Bagnasco M. Soluble CTLA-4 in autoimmune thyroid diseases: relationship with clinical status and possible role in the immune response dysregulation. Clin Immunol. 2007 May;123(2):190-8. (14D3, WB, PubMed)

Vandenborre K, et al. American Journal of Pathology 1998 152: 963-73.

Vandenborre K, et al. Immunology 1999 98: 1-10.

T.L. Walunas, et al Immunity 1994 1: 405-413.

N.J. Karandikar, et al. Journal of Experimental Medicine 1996 184: 783-788.


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