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ABL1 anticorps

Cet anticorps anti-ABL1 est un anticorps Souris Monoclonal détectant ABL1 dans WB, IF et IP. Adapté pour Humain et Souris. Ce Primary Antibody a été cité dans 5+ publications.
N° du produit ABIN967410

Aperçu rapide pour ABL1 anticorps (ABIN967410)

Antigène

Voir toutes ABL1 Anticorps
ABL1 (C-Abl Oncogene 1, Non-Receptor tyrosine Kinase (ABL1))

Reactivité

  • 225
  • 135
  • 97
  • 13
  • 2
  • 1
  • 1
  • 1
  • 1
  • 1
Humain, Souris

Hôte

  • 309
  • 3
Souris

Clonalité

  • 308
  • 4
Monoclonal

Conjugué

  • 112
  • 18
  • 17
  • 15
  • 11
  • 11
  • 11
  • 11
  • 11
  • 11
  • 11
  • 11
  • 11
  • 11
  • 11
  • 9
  • 8
  • 2
  • 2
  • 2
  • 2
  • 2
  • 2
Cet anticorp ABL1 est non-conjugé

Application

  • 213
  • 143
  • 143
  • 122
  • 66
  • 54
  • 34
  • 33
  • 19
  • 18
  • 11
  • 4
  • 3
  • 3
  • 2
  • 1
  • 1
Western Blotting (WB), Immunofluorescence (IF), Immunoprecipitation (IP)

Clone

8E9
  • Marque

    BD Pharmingen™

     Réactivité croisée

    Souris

    Attributs du produit

    1. Since applications vary, each investigator should titrate the reagent to obtain optimal results.
    2. Please refer to us for technical protocols.
    3. Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.

    Purification

    The monoclonal antibody was purified from tissue culture supernatant or ascites by affinity chromatography.

    Immunogène

    Recombinant Mouse Abl Gag Fusion Protein

    Isotype

    IgG1
  • Commentaires

    Related Products: ABIN967389

    Restrictions

    For Research Use only
  • Format

    Liquid

    Concentration

    0.5 mg/mL

    Buffer

    Aqueous buffered solution containing ≤0.09 % sodium azide.

    Agent conservateur

    Sodium azide

    Précaution d'utilisation

    This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

    Stock

    4 °C

    Stockage commentaire

    Store undiluted at 4° C.
  • Guo, Lian, Xian, Lee, Deisseroth, Stass, Champlin, Talpaz, Wang, Arlinghaus: "BCR-ABL protein expression in peripheral blood cells of chronic myelogenous leukemia patients undergoing therapy." dans: Blood, Vol. 83, Issue 12, pp. 3629-37, (1994) (PubMed).

    Guo, Hirsch-Ginsberg, Xian, Stass, Champlin, Giralt, McCredie, Campbell, Arlinghaus: "Acute lymphoid leukemia molecular phenotype in a patient with benign-phase chronic myelogenous leukemia." dans: Hematologic pathology, Vol. 7, Issue 2, pp. 91-106, (1993) (PubMed).

    Guo, Wang, Arlinghaus: "Detection of BCR-ABL proteins in blood cells of benign phase chronic myelogenous leukemia patients." dans: Cancer research, Vol. 51, Issue 11, pp. 3048-51, (1991) (PubMed).

    Wang: "Negative regulation of c-abl tyrosine kinase by its variable N-terminal amino acids." dans: Oncogene research, Vol. 3, Issue 3, pp. 293-8, (1989) (PubMed).

    Kipreos, Lee, Wang: "Isolation of temperature-sensitive tyrosine kinase mutants of v-abl oncogene by screening with antibodies for phosphotyrosine." dans: Proceedings of the National Academy of Sciences of the United States of America, Vol. 84, Issue 5, pp. 1345-9, (1987) (PubMed).

  • Antigène

    ABL1 (C-Abl Oncogene 1, Non-Receptor tyrosine Kinase (ABL1))

    Autre désignation

    Abl

    Sujet

    The proto-oncogene c-abl was first isolated from the mouse genome as a gene with similarity to the v-abl oncogene of Abelson murine leukemia virus. The c-abl gene encodes a protein tyrosine kinase that is localized in the cytoplasm and nucleus. The c-abl protein shares several common features with other cytoplasmic tyrosine kinases, including the src-homology domains 2 (SH2) and 3 (SH3). The SH2 domain is believed to bind specifically to tyrosine residues of other proteins. The function of the SH3 domain is still unclear. Unique to the c-abl tyrosine kinase is a large C-terminal segment which seems to be essential for its biological function, since mice homozygous for a C-terminal deletion of c-abl have multiple defects at birth. The C-terminal fragment of c-abl contains a DNA-binding domain, and the DNA-binding affinity of this domain seems to be regulated by phosphorylation of critical serine/threonine residues. The c-abl proto-oncogene can be activated in a variety of ways. For example, in Philadelphia chromosome (Ph1)-positive leukemias the c-abl proto-oncogene on chromosome 9 becomes fused to the bcr gene on chromosome 22, and bcr-abl fusion proteins are produced. Ph1-positive cells express either the a-typical 210 kDa bcr-abl fusion protein or a smaller 185 kDa bcr-abl fusion protein. The bcr sequences activate the c-abl tyrosine kinase by deregulating its expression, and actin filament-binding function associated with c-abl is also activated. Expression of bcr-abl fusion proteins in vitro leads to transformation of pre-B lymphoid cells supporting their role as an oncogene. The phosphorylated form of c-abl is observed at ~145 kDa on SDS/PAGE. The 8E9 clone has been reported to react with an epitope in the tyrosine kinase domain of murine abl proteins [Wang et al.]. This antibody is routinely tested by western blot analysis.

    Poids moléculaire

    145 kDa

    Pathways

    Apoptose, Regulation of Muscle Cell Differentiation, Platelet-derived growth Factor Receptor Signaling, Lipid Metabolism
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