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HSP 90 (4F10) antibody

RRID:AB_2121191

Antibody ID

AB_2121191

Target Antigen

HSP 90 (4F10) human, human

Proper Citation

(Santa Cruz Biotechnology Cat# sc-69703, RRID:AB_2121191)

Clonality

monoclonal antibody

Comments

validation status unknown check with seller; recommendations: ELISA; Western Blot; Immunoprecipitation; WB, IP, ELISA

Host Organism

mouse

Vendor

Santa Cruz Biotechnology

Cat Num

sc-69703

Publications that use this research resource

Dynamics of PARKIN-Dependent Mitochondrial Ubiquitylation in Induced Neurons and Model Systems Revealed by Digital Snapshot Proteomics.

  • Ordureau A
  • Mol. Cell
  • 2018 Apr 19

Literature context:


Abstract:

Flux through kinase and ubiquitin-driven signaling systems depends on the modification kinetics, stoichiometry, primary site specificity, and target abundance within the pathway, yet we rarely understand these parameters and their spatial organization within cells. Here we develop temporal digital snapshots of ubiquitin signaling on the mitochondrial outer membrane in embryonic stem cell-derived neurons, and we model HeLa cell systems upon activation of the PINK1 kinase and PARKIN ubiquitin ligase by proteomic counting of ubiquitylation and phosphorylation events. We define the kinetics and site specificity of PARKIN-dependent target ubiquitylation, and we demonstrate the power of this approach to quantify pathway modulators and to mechanistically define the role of PARKIN UBL phosphorylation in pathway activation in induced neurons. Finally, through modulation of pS65-Ub on mitochondria, we demonstrate that Ub hyper-phosphorylation is inhibitory to mitophagy receptor recruitment, indicating that pS65-Ub stoichiometry in vivo is optimized to coordinate PARKIN recruitment via pS65-Ub and mitophagy receptors via unphosphorylated chains.

Funding information:
  • Biotechnology and Biological Sciences Research Council - BB/I004815/1(United Kingdom)
  • NIDDK NIH HHS - K01 DK098285()
  • NIGMS NIH HHS - R01 GM067945()

Co-option of an endogenous retrovirus envelope for host defense in hominid ancestors.

  • Blanco-Melo D
  • Elife
  • 2017 Apr 11

Literature context:


Abstract:

Endogenous retroviral sequences provide a molecular fossil record of ancient infections whose analysis might illuminate mechanisms of viral extinction. A close relative of gammaretroviruses, HERV-T, circulated in primates for ~25 million years (MY) before apparent extinction within the past ~8 MY. Construction of a near-complete catalog of HERV-T fossils in primate genomes allowed us to estimate a ~32 MY old ancestral sequence and reconstruct a functional envelope protein (ancHTenv) that could support infection of a pseudotyped modern gammaretrovirus. Using ancHTenv, we identify monocarboxylate transporter-1 (MCT-1) as a receptor used by HERV-T for attachment and infection. A single HERV-T provirus in hominid genomes includes an env gene (hsaHTenv) that has been uniquely preserved. This apparently exapted HERV-T env could not support virion infection but could block ancHTenv mediated infection, by causing MCT-1 depletion from cell surfaces. Thus, hsaHTenv may have contributed to HERV-T extinction, and could also potentially regulate cellular metabolism.