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Homo sapiens


Part of: ENCODE project common cell types; tier 3. Sequence variation: Homozygous for KDR p.Gln472His (c.1416A>T) (from parent cell line). Sequence variation: Homozygous for TP53 p.Tyr220Cys (c.659A>G) (from parent cell line). Omics: Deep proteome analysis. DT Created: 04-04-12; Last updated: 13-11-18; Version: 16

Proper Citation



Cancer cell line DT Created: 04-04-12; Last updated: 13-11-18; Version: 16


DT Created: 04-04-12; Last updated: 13-11-18; Version: 16


Huh 7.5, Huh7.5 DT Created: 04-04-12, Last updated: 13-11-18, Version: 16

Cross References

BTO; BTO:0004126 EFO; EFO_0005704 ENCODE; ENCBS227AAA GEO; GSM816671 Lonza; 1432 PRIDE; PXD006386 Wikidata; Q54896856 DT Created: 04-04-12; Last updated: 13-11-18; Version: 16


DT Created: 04-04-12; Last updated: 13-11-18; Version: 16

Originate from Same Individual

DT Created: 04-04-12; Last updated: 13-11-18; Version: 16

Publications that use this research resource

Diverse Viruses Require the Calcium Transporter SPCA1 for Maturation and Spread.

  • Hoffmann HH
  • Cell Host Microbe
  • 2017 Oct 11

Literature context:


Respiratory and arthropod-borne viral infections are a global threat due to the lack of effective antivirals and vaccines. A potential strategy is to target host proteins required for viruses but non-essential for the host. To identify such proteins, we performed a genome-wide knockout screen in human haploid cells and identified the calcium pump SPCA1. SPCA1 is required by viruses from the Paramyxoviridae, Flaviviridae, and Togaviridae families, including measles, dengue, West Nile, Zika, and chikungunya viruses. Calcium transport activity is required for SPCA1 to promote virus spread. SPCA1 regulates proteases within the trans-Golgi network that require calcium for their activity and are critical for virus glycoprotein maturation. Consistent with these findings, viral glycoproteins fail to mature in SPCA1-deficient cells preventing viral spread, which is evident even in cells with partial loss of SPCA1. Thus, SPCA1 is an attractive antiviral host target for a broad spectrum of established and emerging viral infections.

Funding information:
  • NIDDK NIH HHS - F32 DK095666()
  • NIGMS NIH HHS - GM43644(United States)

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

  • Blanco-Melo D
  • Elife
  • 2017 Apr 11

Literature context:


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.