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BID Protein

Dieses Recombinant BID-Protein wird in Escherichia coli (E. coli) exprimiert.
Produktnummer ABIN7319367

Kurzübersicht für BID Protein (ABIN7319367)

Target

Alle BID Proteine anzeigen
BID (BH3 Interacting Domain Death Agonist (BID))

Protein-Typ

Recombinant

Spezies

  • 12
  • 6
  • 3
  • 1
  • 1
Human

Quelle

  • 12
  • 3
  • 3
  • 2
  • 1
  • 1
Escherichia coli (E. coli)

Reinheit

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

    Recombinant Human BID Protein

    Sequenz

    Met 1-Asp195

    Produktmerkmale

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

    Endotoxin-Niveau

    < 1.0 EU per μg as determined by the LAL method.
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    Produkt
    Expressionssystem
    Konjugat
    Origin
    Preis ab
    Expressionssystem HEK-293 Cells
    Konjugat His tag
    Origin Human
    Preis ab 12.620,45 €
    Expressionssystem Cell-free protein synthesis (CFPS)
    Konjugat Strep Tag
    Origin Human
    Preis ab 15.754,29 €

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  • Beschränkungen

    Nur für Forschungszwecke einsetzbar
  • Format

    Frozen, Liquid

    Buffer

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

    Lagerung

    -20 °C

    Informationen zur Lagerung

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

    BID (BH3 Interacting Domain Death Agonist (BID))

    Andere Bezeichnung

    BID

    Hintergrund

    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

    Molekulargewicht

    22.0 kDa

    Pathways

    Apoptose, Caspase Kaskade in der Apoptose, Positive Regulation of Endopeptidase Activity
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