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Rabbit Anti-gamma H2A.X, phospho (Ser139) Polyclonal Antibody, Unconjugated

RRID:AB_297813

Antibody ID

AB_297813

Target Antigen

gamma H2A.X (phospho S139) human, mouse, reacts with human, mouse and dictyostelium discoideumnot yet tested in other species

Vendor

Abcam

Cat Num

ab11174

Proper Citation

(Abcam Cat# ab11174, RRID:AB_297813)

Reference

PMID:28092266

Clonality

polyclonal antibody

Host Organism

rabbit

Comments

seller recommendations: Immunocytochemistry; Immunofluorescence; Western Blot; Flow Cytometry, Immunocytochemistry, Immunocytochemistry/Immunofluorescence, Western Blot

Publications that use this research resource

Huwe1 Regulates the Establishment and Maintenance of Spermatogonia by Suppressing DNA Damage Response.

  • Fok KL
  • Endocrinology
  • 2017 Nov 1

Literature context: it; polyclonal 1:2000 1:2500 RRID:AB_297813


Abstract:

Spermatogenesis is sustained by a heterogeneous population of spermatogonia that includes the spermatogonial stem cells. However, the mechanisms underlying their establishment from gonocyte embryonic precursors and their maintenance thereafter remain largely unknown. In this study, we report that inactivation of the ubiquitin ligase Huwe1 in male germ cells in mice led to the degeneration of spermatogonia in neonates and resulted in a Sertoli cell-only phenotype in the adult. Huwe1 knockout gonocytes showed a decrease in mitotic re-entry, which inhibited their transition to spermatogonia. Inactivation of Huwe1 in primary spermatogonial culture or the C18-4 cell line resulted in cell degeneration. Degeneration of Huwe1 knockout spermatogonia was associated with an increased level of histone H2AX and an elevated DNA damage response that led to apparent mitotic catastrophe but not apoptosis or senescence. Blocking this increase in H2AX prevented the degeneration of Huwe1-depleted cells. Taken together, these results reveal a previously undefined role of Huwe1 in orchestrating the physiological DNA damage response in the male germline that contributes to the establishment and maintenance of spermatogonia.

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

Literature context: ab11174 (RRID:AB_297813)


Abstract:

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.

Funding information:
  • NCI NIH HHS - P01 CA129243()
  • NCI NIH HHS - P30 CA045508()