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MABT203

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

clone 24-21, from mouse

Synonym(s):

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
NACRES:
NA.41
eCl@ss:
32160702

Key Documents

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Product Name

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

biological source

mouse

conjugate

unconjugated

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.

NP_005148

UniProt accession no.

P00519

shipped in

wet ice

target post-translational modification

unmodified

Quality Level

100

Gene Information

human ... ABI1(10006)

Analysis Note

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.

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.).

Biochem/physiol Actions

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

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.
~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.

Immunogen

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

Other Notes

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

Physical form

Format: Purified

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Storage Class

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘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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