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BAD antibody (pThr94)

This Rabbit Polyclonal antibody specifically detects BAD in DB. It exhibits reactivity toward Mouse and has been mentioned in 5+ publications.
Catalog No. ABIN1881097

Quick Overview for BAD antibody (pThr94) (ABIN1881097)

Target

See all BAD Antibodies
BAD (BCL2-Associated Agonist of Cell Death (BAD))

Reactivity

  • 365
  • 214
  • 139
  • 19
  • 10
  • 7
  • 4
  • 4
  • 3
  • 2
  • 1
  • 1
  • 1
  • 1
  • 1
Mouse

Host

  • 431
  • 14
  • 1
Rabbit

Clonality

  • 415
  • 31
Polyclonal

Conjugate

  • 181
  • 38
  • 35
  • 35
  • 32
  • 29
  • 6
  • 6
  • 6
  • 6
  • 6
  • 6
  • 6
  • 6
  • 6
  • 6
  • 6
  • 5
  • 5
  • 5
  • 5
  • 5
  • 5
This BAD antibody is un-conjugated

Application

  • 256
  • 233
  • 162
  • 93
  • 81
  • 80
  • 54
  • 51
  • 23
  • 21
  • 14
  • 12
  • 10
  • 2
  • 2
  • 1
  • 1
  • 1
  • 1
  • 1
Dot Blot (DB)

Clone

RB39418
  • Binding Specificity

    • 35
    • 33
    • 27
    • 25
    • 23
    • 23
    • 22
    • 22
    • 15
    • 8
    • 8
    • 8
    • 8
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    • 8
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    • 7
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    • 7
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    • 6
    • 5
    • 4
    • 4
    • 4
    • 3
    • 3
    • 2
    • 2
    • 2
    • 2
    • 2
    • 2
    • 2
    • 2
    • 2
    • 1
    • 1
    • 1
    • 1
    pThr94

    Purification

    This antibody is purified through a protein A column, followed by peptide affinity purification.

    Immunogen

    This mouse BAD Antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding T94 of mouse BAD.

    Isotype

    Ig Fraction
  • Application Notes

    DB: 1:500

    Restrictions

    For Research Use only
  • Format

    Liquid

    Buffer

    Purified polyclonal antibody supplied in PBS with 0.09 % (W/V) sodium azide.

    Preservative

    Sodium azide

    Precaution of Use

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

    Storage

    4 °C,-20 °C

    Expiry Date

    6 months
  • Kim, Xin, Moioli, Chung, Lee, Chen, Fu, Koch, Mao: "Regeneration of dental-pulp-like tissue by chemotaxis-induced cell homing." in: Tissue engineering. Part A, Vol. 16, Issue 10, pp. 3023-31, (2010) (PubMed).

    Frenzel, Labi, Chmelewskij, Ploner, Geley, Fiegl, Tzankov, Villunger: "Suppression of B-cell lymphomagenesis by the BH3-only proteins Bmf and Bad." in: Blood, Vol. 115, Issue 5, pp. 995-1005, (2010) (PubMed).

    Quoyer, Longuet, Broca, Linck, Costes, Varin, Bockaert, Bertrand, Dalle: "GLP-1 mediates antiapoptotic effect by phosphorylating Bad through a beta-arrestin 1-mediated ERK1/2 activation in pancreatic beta-cells." in: The Journal of biological chemistry, Vol. 285, Issue 3, pp. 1989-2002, (2010) (PubMed).

    Wu, Wang, Schroer, Choi, Chen, Okada, Woo: "Perinatal survivin is essential for the establishment of pancreatic beta cell mass in mice." in: Diabetologia, Vol. 52, Issue 10, pp. 2130-41, (2009) (PubMed).

    Polzien, Baljuls, Rennefahrt, Fischer, Schmitz, Zahedi, Sickmann, Metz, Albert, Benz, Hekman, Rapp: "Identification of novel in vivo phosphorylation sites of the human proapoptotic protein BAD: pore-forming activity of BAD is regulated by phosphorylation." in: The Journal of biological chemistry, Vol. 284, Issue 41, pp. 28004-20, (2009) (PubMed).

  • Target

    BAD (BCL2-Associated Agonist of Cell Death (BAD))

    Alternative Name

    BAD

    Background

    Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways.

    Molecular Weight

    22080

    NCBI Accession

    NP_031548

    UniProt

    Q61337

    Pathways

    MAPK Signaling, PI3K-Akt Signaling, RTK Signaling, Apoptosis, Fc-epsilon Receptor Signaling Pathway, Positive Regulation of Peptide Hormone Secretion, Carbohydrate Homeostasis, Positive Regulation of Endopeptidase Activity, Regulation of Carbohydrate Metabolic Process, Hepatitis C, CXCR4-mediated Signaling Events
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