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BID Protéine

Cette protéine Recombinant BID est exprimée dans Escherichia coli (E. coli).
N° du produit ABIN7319367

Aperçu rapide pour BID Protéine (ABIN7319367)

Antigène

Voir toutes BID Protéines
BID (BH3 Interacting Domain Death Agonist (BID))

Type de proteíne

Recombinant

Origine

  • 11
  • 5
  • 3
  • 1
  • 1
Humain

Source

  • 10
  • 3
  • 3
  • 2
  • 1
  • 1
Escherichia coli (E. coli)

Pureté

> 95 % as determined by reducing SDS-PAGE.
  • Fonction

    Recombinant Human BID Protein

    Séquence

    Met 1-Asp195

    Attributs du produit

    Recombinant Human BH3-Interacting Domain Death Agonist is produced by our E.coli expression system and the target gene encoding Met1-Asp195 is expressed.

    niveau d'endotoxine

    < 1.0 EU per μg as determined by the LAL method.
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    Produit
    Système d'expression
    Conjugué
    Origin
    Prix à partir de
    Système d'expression HEK-293 Cells
    Conjugué His tag
    Origin Human
    Prix à partir de 12.620,45 €
    Système d'expression Cell-free protein synthesis (CFPS)
    Conjugué Strep Tag
    Origin Human
    Prix à partir de 20.480,57 €

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  • Restrictions

    For Research Use only
  • Format

    Frozen, Liquid

    Buffer

    Supplied as a 0.2 μm filtered solution of 20 mM PB, 100 mM KCl, pH 7.4.

    Stock

    -20 °C

    Stockage commentaire

    Store at < -20°C, stable for 6 months. Please minimize freeze-thaw cycles.
  • Antigène

    BID (BH3 Interacting Domain Death Agonist (BID))

    Autre désignation

    BID

    Sujet

    Background: BH3-Interacting Domain Death Agonist (BID) is a member of the Bcl-2 protein family which regulates outer mitochondrial membrane permeability. BID is a pro-apoptotic member that causes cytochrome c to be released from the mitochondria intermembrane space into the cytosol. Interaction of Bid with Bak causes altered mitochondrial membrane permeability. BID contains only the BH3 domain, which is required for its interaction with the Bcl-2 family proteins and for its pro-death activity. BID is susceptible to proteolytic cleavage by caspases, calpains, Granzyme B and cathepsins. It is an integrating key regulator of the intrinsic death pathway that amplifies caspase-dependent and caspase-independent execution of neuronal apoptosis. Therefore pharmacological inhibition of BID provides a promising therapeutic strategy in neurological diseases where programmed cell death is prominent, and also offer a new strategy for the treatment of acute renal failure associated with ischemia-reperfusion. BID receives direct inputs from a key regulator of the cell cycle arrest/DNA repair machinery (ATM), and therefore is an excellent candidate to coordinate genotoxic stress responses and apoptotic cell death. BID is a novel pro-apoptosis Bcl-2 family protein that is activated by caspase 8 in response to Fas/TNF-R1 death receptor signals. Deletion of BID inhibits carcinogenesis in the liver, although this genetic alteration promotes tumorigenesis in the myeloid cells. This is likely related to the function of BID to promote cell cycle progression into S phase. BID could be also involved in the maintenance of genomic stability by engaging at mitosis checkpoint.

    Synonym: BH3-Interacting Domain Death Agonist, p22 BID, BID

    Poids moléculaire

    22.0 kDa

    Pathways

    Apoptose, Caspase Cascade in Apoptosis, Positive Regulation of Endopeptidase Activity
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