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SF7761

RRID:CVCL_IT45

Organism

Homo sapiens

Comments

Doubling time: 48 hours (PubMed=22983601). Sequence variation: H3F3A p.Lys28Met (c.83A>T) (H3.3K27M) (PubMed=23603901). Transfected with: HGNC; 11730; TERT. Omics: CNV analysis. Omics: Deep RNAseq analysis. Omics: Transcriptome analysis. DT Created: 03-03-17; Last updated: 07-09-18; Version: 5

Proper Citation

Millipore Cat# SCC126, RRID:CVCL_IT45

Category

Telomerase immortalized cell line DT Created: 03-03-17; Last updated: 07-09-18; Version: 5

Sex

DT Created: 03-03-17; Last updated: 07-09-18; Version: 5

Synonyms

DT Created: 03-03-17, Last updated: 07-09-18, Version: 5

Vendor

Millipore

Cat Num

SCC126

Cross References

Cosmic; 1925952 GEO; GSM1508943 GEO; GSM1508944 GEO; GSM1508945 GEO; GSM1508946 GEO; GSM1508947 GEO; GSM1508948 GEO; GSM1508951 Millipore; SCC126 Wikidata; Q54952936 DT Created: 03-03-17; Last updated: 07-09-18; Version: 5

Hierarchy

DT Created: 03-03-17; Last updated: 07-09-18; Version: 5

Originate from Same Individual

DT Created: 03-03-17; Last updated: 07-09-18; Version: 5

Publications that use this research resource

H3.3K27M mutant proteins reprogram epigenome by sequestering the PRC2 complex to poised enhancers.

  • Fang D
  • Elife
  • 2018 Jun 22

Literature context:


Abstract:

Expression of histone H3.3K27M mutant proteins in human diffuse intrinsic pontine glioma (DIPG) results in a global reduction of tri-methylation of H3K27 (H3K27me3), and paradoxically, H3K27me3 peaks remain at hundreds of genomic loci, a dichotomous change that lacks mechanistic insights. Here, we show that the PRC2 complex is sequestered at poised enhancers, but not at active promoters with high levels of H3.3K27M proteins, thereby contributing to the global reduction of H3K27me3. Moreover, the levels of H3.3K27M proteins are low at the retained H3K27me3 peaks and consequently having minimal effects on the PRC2 activity at these loci. H3K27me3-mediated silencing at specific tumor suppressor genes, including Wilms Tumor 1, promotes proliferation of DIPG cells. These results support a model in which the PRC2 complex is redistributed to poised enhancers in H3.3K27M mutant cells and contributes to tumorigenesis in part by locally enhancing H3K27me3, and hence silencing of tumor suppressor genes.

Funding information:
  • National Institutes of Health - CA204297()
  • NIGMS NIH HHS - GM107466(United States)