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M. dunni (Clone III8C)

RRID:CVCL_9125

Organism

Mus terricolor

Comments

DT Created: 06-06-12; Last updated: 25-02-19; Version: 8

Proper Citation

ATCC Cat# CRL-2017, RRID:CVCL_9125

Reference

PMID:6092693

Category

Spontaneously immortalized cell line DT Created: 06-06-12; Last updated: 25-02-19; Version: 8

Sex

DT Created: 06-06-12; Last updated: 25-02-19; Version: 8

Synonyms

M. dunni clone III8C, M.dunni(Clone III8C), Clone IIIC8 DT Created: 06-06-12, Last updated: 25-02-19, Version: 8

Vendor

ATCC

Cat Num

CRL-2017

Cross References

CLO; CLO_0007440 CLO; CLO_0007441 CLDB; cl3306 ATCC; CRL-2017 BCRC; 60203 ECACC; 94101211 JCRB; JCRB9124 Wikidata; Q54903377 DT Created: 06-06-12; Last updated: 25-02-19; Version: 8

Hierarchy

DT Created: 06-06-12; Last updated: 25-02-19; Version: 8

Originate from Same Individual

DT Created: 06-06-12; Last updated: 25-02-19; Version: 8

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.