Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Replication-dependent downregulation of cellular angiotensin-converting enzyme 2 protein expression by human coronavirus NL63

21 Jun 2012

Abstract excerpt

Like severe acute respiratory syndrome coronavirus (SARS-CoV), human coronavirus (HCoV)-NL63 employs angiotensin-converting enzyme 2 (ACE2) as a receptor for cellular entry. SARS-CoV infection causes robust downregulation of cellular ACE2 expression levels and it has been suggested that the SARS-CoV effect on ACE2 is involved in the severity of disease. We investigated whether cellular ACE2 downregulation occurs...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to COVID-19 Clinical Research Studies
Share to Renin-Angiotensin System Studies
Share to SARS-CoV-2 and COVID-19 Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 22718567
DOI: 10.1099/vir.0.043919-0

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Replication-dependent downregulation of cellular angiotensin-converting enzyme 2 protein expression by human coronavirus NL63PMID 22718567Read ↗

Differential Downregulation of ACE2 by the Spike Proteins of Severe Acute Respiratory Syndrome Coronavirus and Human Coronavirus NL63Semantic proximity Read ↗

Human coronavirus NL63 employs the severe acute respiratory syndrome coronavirus receptor for cellular entrySemantic proximity Read ↗

Seasonal human coronaviruses OC43, 229E, and NL63 induce cell surface modulation of entry receptors and display host cell-specific viral replication kineticsSemantic proximity Read ↗

Seasonal Human Coronaviruses OC43, 229E, and NL63 Induce Cell Surface Modulation of Entry Receptors and Display Host Cell-Specific Viral Replication KineticsSemantic proximity Read ↗

Crystal structure of NL63 respiratory coronavirus receptor-binding domain complexed with its human receptorSemantic proximity Read ↗

Human Coronavirus EMC Does Not Require the SARS-Coronavirus Receptor and Maintains Broad Replicative Capability in Mammalian Cell LinesSemantic proximity Read ↗

Interaction between the spike protein of human coronavirus NL63 and its cellular receptor ACE2.Semantic proximity Read ↗

Development of an in Vitro Model to Investigate the Regulation of ACE2 Expression and its Correlation with ACE2-Mediated Viral EntrySemantic proximity Read ↗

Highly Conserved Regions within the Spike Proteins of Human Coronaviruses 229E and NL63 Determine Recognition of Their Respective Cellular ReceptorsSemantic proximity Read ↗

MRC5 cells engineered to express ACE2 serve as a model system for the discovery of antivirals targeting SARS-CoV-2Semantic proximity Read ↗

The Nasal Symbiont <i>Staphylococcus Epidermidis</i> Restricts the Transcription of SARS-CoV-2 Entry Factors in Human Nasal EpitheliumSemantic proximity Read ↗

The nasal symbiont Staphylococcus epidermidis shapes the cellular environment to decrease expression of SARS-CoV-2 entry factors in nasal epitheliumSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.