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Tag: SMR peptide antagonizes mortalin promoted release of extracellular vesicles and affects mortalin protection from complement-dependent cytotoxicity in breast cancer cells and leukemia cells.

SMR peptide antagonizes mortalin promoted release of extracellular vesicles and affects mortalin protection from complement-dependent cytotoxicity in breast cancer cells and leukemia cells.

SMR peptide antagonizes mortalin promoted release of extracellular vesicles and affects mortalin protection from complement-dependent cytotoxicity in breast cancer cells and leukemia cells.

Posted on May 10, 2020May 10, 2020 by Frank

Background: Mortalin/GRP-75/mt-hsp70 is a mitochondrial chaperone protein, discovered in the cytoplasm, endoplasmic reticulum and cytoplasmic vesicles. It features in many mobile processes similar to mitochondrial biogenesis, intramobile trafficking, cell proliferation, signaling, immortalization and tumorigenesis. Thus, inhibition of mortalin is a promising avenue for cancer remedy. Previous research in our lab have recommended that mortalin contributes to breast cancer improvement and development.… Continue reading

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  • People with disability and privacy in precision medicine research: what’s at stake?
  • Complexities of mammalian transcriptome revealed by targeted RNA enrichment techniques
  • Clinical progress in genome-editing technology and in vivo delivery techniques
  • Polygenic sex determination in vertebrates – is there any such thing?
  • Emerging regulatory mechanisms of noncoding RNAs in topologically associating domains
  • RNA out of the mist
  • Consequences of trisomy syndromes – 21 and beyond
  • A proposed metric set for evaluation of genome assembly quality
  • Host genetic variability and determinants of severe COVID-19

Categories

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  • 96T
  • apoptosis
  • array
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  • Bacteria
  • DNA
  • Establishment and characterization of HBV-associated B lymphocytes with an immortalization potential.
  • GMO
  • Goat
  • Green
  • Guinea
  • Malignant transformation in a Breast Adenomyoepithelioma Caused by Amplification of c-MYC: A Common pathway to Cancer in a Rare Entity.
  • Mechanisms underlying the activation of TERT transcription and telomerase activity in human cancer: old actors and new players.
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  • Plant
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