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FRhK-4

RRID:CVCL_4522

Organism

Macaca mulatta

Comments

Group: Non-human primate cell line. DT Created: 04-04-12; Last updated: 06-09-19; Version: 12

Proper Citation

IZSLER Cat# BS CL 115, RRID:CVCL_4522

Reference

PMID:4633070

Category

Spontaneously immortalized cell line DT Created: 04-04-12; Last updated: 06-09-19; Version: 12

Sex

DT Created: 04-04-12; Last updated: 06-09-19; Version: 12

Synonyms

FRHK-4, Frhk-4, FRhK4, Fetal Rhesus Kidney-4 DT Created: 04-04-12, Last updated: 06-09-19, Version: 12

Vendor

IZSLER

Cat Num

BS CL 115

Cross References

CLO; CLO_0003388 CLDB; cl1385 ATCC; CRL-1688 BCRC; 60095 CCRID; 3131C0001000400018 CCRID; 3142C0001000000036 CCTCC; GDC0036 IZSLER; BS CL 115 Wikidata; Q54835161 DT Created: 04-04-12; Last updated: 06-09-19; Version: 12

Hierarchy

DT Created: 04-04-12; Last updated: 06-09-19; Version: 12

Originate from Same Individual

DT Created: 04-04-12; Last updated: 06-09-19; Version: 12

Publications that use this research resource

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.

Ebola Virus Glycoprotein with Increased Infectivity Dominated the 2013-2016 Epidemic.

  • Diehl WE
  • Cell
  • 2016 Nov 3

Literature context:


Abstract:

The magnitude of the 2013-2016 Ebola virus disease (EVD) epidemic enabled an unprecedented number of viral mutations to occur over successive human-to-human transmission events, increasing the probability that adaptation to the human host occurred during the outbreak. We investigated one nonsynonymous mutation, Ebola virus (EBOV) glycoprotein (GP) mutant A82V, for its effect on viral infectivity. This mutation, located at the NPC1-binding site on EBOV GP, occurred early in the 2013-2016 outbreak and rose to high frequency. We found that GP-A82V had heightened ability to infect primate cells, including human dendritic cells. The increased infectivity was restricted to cells that have primate-specific NPC1 sequences at the EBOV interface, suggesting that this mutation was indeed an adaptation to the human host. GP-A82V was associated with increased mortality, consistent with the hypothesis that the heightened intrinsic infectivity of GP-A82V contributed to disease severity during the EVD epidemic.