Overview

  • Product name

  • Description

    Rabbit polyclonal to BACH1/BRIP1
  • Host species

    Rabbit
  • Tested applications

    Suitable for: WB, IP, ICC/IFmore details
  • Species reactivity

    Reacts with: Mouse, Rat, Human
  • Immunogen

    Synthetic peptide:

    NFKPSPSKNKGMFPGFK

    conjugated to KLH by a N terminal Cysteine residue linker, corresponding to amino acids 1233-1249 of Human BACH1/BRIP1

  • Positive control

    • Whole extract of human MCF-7 cells, whole extracts of mouse NIH-3T3 and rat PC12 cells and RIPA extract of human HeLa cells.

Properties

Applications

Our Abpromise guarantee covers the use of ab49657 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
WB Use a concentration of 0.1 - 1 µg/ml. Predicted molecular weight: 150 kDa.
IP Use a concentration of 1 - 10 µg/ml.
ICC/IF Use a concentration of 10 - 20 µg/ml.

Target

  • Function

    DNA-dependent ATPase and 5' to 3' DNA helicase required for the maintenance of chromosomal stability. Acts late in the Fanconi anemia pathway, after FANCD2 ubiquitination. Involved in the repair of DNA double-strand breaks by homologous recombination in a manner that depends on its association with BRCA1.
  • Tissue specificity

    Ubiquitously expressed, with highest levels in testis.
  • Involvement in disease

    Defects in BRIP1 are a cause of susceptibility to breast cancer (BC) [MIM:114480]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case.
    Defects in BRIP1 are the cause of Fanconi anemia complementation group J (FANCJ) [MIM:609054]. It is a disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.
  • Sequence similarities

    Belongs to the DEAD box helicase family. DEAH subfamily.
    Contains 1 helicase ATP-binding domain.
  • Domain

    4Fe-4S iron-sulfur-binding is required for helicase activity (PubMed:20639400).
  • Post-translational
    modifications

    Phosphorylated. Phosphorylation is necessary for interaction with BRCA1, and is cell-cycle regulated.
  • Cellular localization

    Nucleus.
  • Information by UniProt
  • Database links

  • Alternative names

    • ATP dependent RNA helicase BRIP1 antibody
    • ATP-dependent RNA helicase BRIP1 antibody
    • BACH 1 antibody
    • BRAC 1 Associated C Terminal Helicase 1 antibody
    • BRCA 1 Interacting Protein 1 antibody
    • BRCA1 binding helicase like protein BACH1 antibody
    • BRCA1 interacting protein C terminal helicase 1 antibody
    • BRCA1-associated C-terminal helicase 1 antibody
    • BRCA1-interacting protein 1 antibody
    • BRCA1-interacting protein C-terminal helicase 1 antibody
    • BRCA1/BRCA2 associated helicase 1 antibody
    • BRIP 1 antibody
    • BRIP1 antibody
    • FANCJ antibody
    • FANCJ_HUMAN antibody
    • Fanconi anemia group J protein antibody
    • FLJ90232 antibody
    • MGC126521 antibody
    • MGC126523 antibody
    • OF antibody
    • Protein FACJ antibody
    see all

References

This product has been referenced in:

  • Li X  et al. Inhibition of AZIN2-sv induces neovascularization and improves prognosis after myocardial infarction by blocking ubiquitin-dependent talin1 degradation and activating the Akt pathway. EBioMedicine N/A:N/A (2018). Read more (PubMed: 30545799) »
  • Liu Y & Zheng Y Bach1 siRNA attenuates bleomycin-induced pulmonary fibrosis by modulating oxidative stress in mice. Int J Mol Med 39:91-100 (2017). WB . Read more (PubMed: 27959382) »
See all 3 Publications for this product

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