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Merck

A4355

Sigma-Aldrich

Monoclonal Anti-ASPP1 antibody produced in mouse

~2 mg/mL, clone LXO54.2, purified immunoglobulin, buffered aqueous solution

Sinónimos:

Anti-Apoptosis-stimulating protein of p53, 1, Anti-PPP1R13B, Anti-protein phosphatase 1 regulatory subunit 13B

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

LXO54.2, monoclonal

form

buffered aqueous solution

mol wt

antigen ~175 kDa

species reactivity

mouse, human

concentration

~2 mg/mL

technique(s)

immunoprecipitation (IP): suitable
microarray: suitable
western blot: 1-2 μg/mL using total cell extract of human osteogenic sarcoma, U-2-OS

isotype

IgG1

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

General description

ASPP1 interacts with p53 to enhance p53-induced apoptosis.
Monoclonal Anti-ASPP1 (mouse IgG1 isotype) is derived from the hybridoma LXO54.2 produced by the fusion of mouse myeloma cells (SP2/0 cells) and splenocytes from BALB/c mice immunized with a recombinant fragment of human ASPP1, amino acids. Apoptosis-stimulating protein of p53, 1 (ASPP1) belongs to the ASPP family of proteins. This protein contains a proline-rich region, four ankyrin repeats, and an SH3 domain in the C-terminal end.

Immunogen

recombinant fragment of human ASPP1 (amino acids 1-308).

Application

Monoclonal Anti-ASPP1 antibody can be used for western blot at 1-2 μg/mL using total cell extract of human osteogenic sarcoma, U-2-OS. The antibody can also be used for microarray and immunoprecipitation assays.

Biochem/physiol Actions

Apoptosis-stimulating protein of p53, 1 (ASPP1) is known to stimulate RAS signalling which subsequently enhances p53-dependent apoptosis in cancer cells. Furthermore, ASPP1 can also induce p53-independent apoptosis by enhancing the apoptotic functions of p63 and p73. Monoclonal Anti-ASPP1 antibody recognizes human and mouse ASPP1.

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Disclaimer

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.

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Descripción
Precios

Storage Class

10 - Combustible liquids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


Certificados de análisis (COA)

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Xingwen Wang et al.
International journal of cancer, 141(7), 1422-1433 (2017-06-29)
Inactivation of p53 has been shown to correlate with drug resistance in tumors. However, in clear cell renal cell carcinoma (ccRCC), p53 is rarely mutated, yet the tumors remain highly insensitive to the conventional chemotherapeutic drugs. The underlying mechanisms responsible
Daniele Bergamaschi et al.
Molecular and cellular biology, 24(3), 1341-1350 (2004-01-20)
We recently showed that ASPP1 and ASPP2 stimulate the apoptotic function of p53. We show here that ASPP1 and ASPP2 also induce apoptosis independently of p53. By binding to p63 and p73 in vitro and in vivo, ASPP1 and ASPP2
V Fogal et al.
Cell death and differentiation, 12(4), 369-376 (2005-02-26)
The E2F family of transcription factors regulates the expression of a number of genes whose products are involved in cell cycle control, DNA replication and apoptosis. We show here that E2F-1 binds in vivo the promoters of ASPP1 and ASPP2
ASPP1 and ASPP2 are new transcriptional targets of E2F
Fogal V, et al.
Cell Death and Differentiation, 12(4), 369-369 (2005)
ASPP proteins specifically stimulate the apoptotic function of p53
Samuels-Lev Y, et al.
Molecular Cell, 8(4), 781-794 (2001)

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