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Key Documents

MABT203

Sigma-Aldrich

Anti-Abl (c-, v-, Bcr-) Antibody, clone 24-21

clone 24-21, from mouse

Sinónimos:

Tyrosine-protein kinase ABL1, Abelson murine leukemia viral oncogene homolog 1, Abelson tyrosine-protein kinase 1, Proto-oncogene c-Abl, p150

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

purified antibody

antibody product type

primary antibodies

clone

24-21, monoclonal

species reactivity

human

technique(s)

immunocytochemistry: suitable
western blot: suitable

isotype

IgG1κ

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... ABI1(10006)

General description

c-Abl, v-Abl, and Bcr-abl are ubiquitously expressed non-receptor tyrosine kinases that are involved in a plethora of cellular processes. c-Abl is involved in cytoskeleton remodeling and facilitates cell adhesion and cell motility. c-Abl achieves cytoskeleton remodeling by phosphorylating and activating a wide variety of cytoskeleton-associated proteins such as WASF3, ANXA1, DBN1, DBNL, CTTN, RAPH1, ENAH, MAPT, and PXN. Abl-1 also phosphorylates a number of receptor tyrosine kinases and is involved in regulating levels of EGFR by endocytosis. c-Abl may also play a role in DNA damage response via the ATM pathway, among other cellular processes. Whereas v-Abl is known to be involved in pre-B cell transformation in mice, Bcr-Abl is reported to promote cellular growth in leukemia cells and maintain CML phenotype. Many v-Abl- and Bcr-abl-mediated signaling events have been described; however the complexity and function of these pathways require further elucidation.

Specificity

This antibody recognizes the c-terminus of c-Abl, v-Abl, and Bcr-Abl.

Immunogen

Recombinant protein corresponding to the carboxyl region of human v-Abl fused with TrpE.

Application

Anti-Abl (c-, v-, Bcr-) Antibody, clone 24-21 detects level of Abl (c-, v-, Bcr-), clone 24-21 & has been published & validated for use in Western Blotting, ICC.
Immunocytochemistry Analysis: A representative lot from an independent laboratory detected Abl (c-, v-, Bcr-) in COS-7 and 7C411 cells (Goga, A., et al. (1993). Mol Cell Biol. 13(8):4967-49775.).

Quality

Evaluated by Western Blot in K562 cell lysate.

Western Blot Analysis: 1 µg/mL of this antibody detected Abl (c-, v-, Bcr-) in 10 µg of K562 cell lysate.

Target description

~125 kDa and ~190 kDa observed. Uniprot describes a molecular weight of c-Abl at ~122 kDa Uniprot describes that this protein is subject to post-translational modification. This antibody detected c-Abl (~125 kDa) and Bcr-Abl (~190 kDa) in K562 cell lysate. An uncharacterized band at ~27 kDa may be observed in some cell lysates.

Physical form

Format: Purified

Other Notes

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

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Storage Class

12 - Non Combustible Liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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F Belloc et al.
Cell death and differentiation, 4(8), 806-814 (2006-02-09)
Apoptosis was studied in parental and mdr-1 expressing U937, HL60 and K562 myeloid leukemic cell lines using mdr unrelated inducers of apoptosis such as Ara-C, cycloheximide, serum deprivation, ceramide, monensin and UV irradiation. Apoptosis was efficiently induced by all these
Abelson interactor 1 (ABI1) and its interaction with Wiskott-Aldrich syndrome protein (wasp) are critical for proper eye formation in Xenopus embryos.
Singh, A; Winterbottom, EF; Ji, YJ; Hwang, YS; Daar, IO
The Journal of Biological Chemistry null
Giovanni Amabile et al.
Nature communications, 6, 7091-7091 (2015-05-23)
Chronic myeloid leukaemia (CML) is a myeloproliferative disorder characterized by the genetic translocation t(9;22)(q34;q11.2) encoding for the BCR-ABL fusion oncogene. However, many molecular mechanisms of the disease progression still remain poorly understood. A growing body of evidence suggests that the

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