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Anti-BLM antibody produced in rabbit

RRID:AB_1845372

Antibody ID

AB_1845372

Target Antigen

BLM antibody produced in rabbit human, human

Vendor

Sigma-Aldrich

Cat Num

HPA005689

Proper Citation

(Sigma-Aldrich Cat# HPA005689, RRID:AB_1845372)

Reference

PMID:28092266

Clonality

polyclonal antibody

Host Organism

rabbit

Comments

manufacturer recommendations: Other; Immunohistochemistry; indirect immunofluorescence: suitable, protein array: suitable, immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable

Publications that use this research resource

TGF-β reduces DNA ds-break repair mechanisms to heighten genetic diversity and adaptability of CD44+/CD24- cancer cells.

  • Pal D
  • Elife
  • 2017 Jan 16

Many lines of evidence have indicated that both genetic and non-genetic determinants can contribute to intra-tumor heterogeneity and influence cancer outcomes. Among the best described sub-population of cancer cells generated by non-genetic mechanisms are cells characterized by a CD44+/CD24- cell surface marker profile. Here, we report that human CD44+/CD24- cancer cells are genetically highly unstable because of intrinsic defects in their DNA-repair capabilities. In fact, in CD44+/CD24- cells, constitutive activation of the TGF-beta axis was both necessary and sufficient to reduce the expression of genes that are crucial in coordinating DNA damage repair mechanisms. Consequently, we observed that cancer cells that reside in a CD44+/CD24- state are characterized by increased accumulation of DNA copy number alterations, greater genetic diversity and improved adaptability to drug treatment. Together, these data suggest that the transition into a CD44+/CD24- cell state can promote intra-tumor genetic heterogeneity, spur tumor evolution and increase tumor fitness.