Label-Free Quantitative Proteomics Reveals Survival Mechanisms Developed by Hypertrophic Chondrocytes under ER Stress

Kudelko, Mateusz; Chan, Cecilia W. L.; Sharma, Rakesh; Yao, Qing; Lau, Edward; Chu, Ivan K.; Cheah, Kathryn S. E.; Tanner, Julian A.; Chan, Danny;
  • Publisher: Figshare
  • Related identifiers: doi: 10.1021/acs.jproteome.5b00537.s001, doi: 10.1021/acs.jproteome.5b00537.s002, doi: 10.1021/acs.jproteome.5b00537.s003, doi: 10.1021/acs.jproteome.5b00537.s004
  • Subject: Molecular Biology | ATDC 5 cell lines | Genetics | Pathway enrichment analyses | MCDS | mitochondrial calcium channels | metaphyseal chondrodysplasia type Schmid | 13 del HCs | ER stress | Developmental Biology | Physiology | collagen X proteins | Medicine | growth plate changes | 13 del chondrocytes | mass spectrometry approach | Cell Biology | 13 del collagen X | ER StressEmerging evidence implicates ER stress | Biochemistry | 13 del growth plates | Cancer | mitochondrial membrane polarity
    • FOR: 69999 Biological Sciences not elsewhere classified | 39999 Chemical Sciences not elsewhere classified
    mesheuropmc: sense organs

Emerging evidence implicates ER stress caused by unfolded mutant proteins in chondrocytes as the underlying pathology of chondrodysplasias. ER stress is triggered in hypertrophic chondrocytes (HCs) in a mouse model (13del) of metaphyseal chondrodysplasia typ... View more
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