Pages that link to "Q100750026"
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The following pages link to Neuropilin-1 is a host factor for SARS-CoV-2 infection (Q100750026):
Displaying 50 items.
- Free fatty acid binding pocket in the locked structure of SARS-CoV-2 spike protein (Q99593526) (← links)
- SARS-CoV-2 Spike protein co-opts VEGF-A/Neuropilin-1 receptor signaling to induce analgesia (Q100427774) (← links)
- FURIN Mediated SARS-CoV-2 Spike Protein Cleavage and Endocytosis (Q101210487) (← links)
- TMPRSS2 Mediated SARS-CoV-2 Spike Protein Cleavage and Endocytosis (Q101210488) (← links)
- CD147-spike protein is a novel route for SARS-CoV-2 infection to host cells (Q104073430) (← links)
- Spike Protein of SARS-CoV-2 Activates Macrophages and Contributes to Induction of Acute Lung Inflammations in Mice (Q104438055) (← links)
- Neuropilin-1 is a host factor for SARS-CoV-2 infection (Q104440536) (← links)
- Type I and III IFN-mediated antiviral actions counteracted by SARS-CoV-2 proteins and host inherited factors (Q106452526) (← links)
- SARS-CoV-2 cell-to-cell infection is resistant to neutralizing antibodies (Q107071807) (← links)
- AXL is a candidate receptor for SARS-CoV-2 that promotes infection of pulmonary and bronchial epithelial cells (Q107073621) (← links)
- SARS-CoV-2 infects human pancreatic β cells and elicits β cell impairment (Q107101727) (← links)
- SARS-CoV-2 exacerbates proinflammatory responses in myeloid cells through C-type lectin receptors and Tweety family member 2 (Q107344282) (← links)
- Cell entry by SARS-CoV-2 (Q107392240) (← links)
- Glycosylation of SARS-CoV-2: structural and functional insights (Q107466751) (← links)
- SARS-CoV-2 infects cells after viral entry via clathrin-mediated endocytosis (Q107473200) (← links)
- The Polybasic Cleavage Site in SARS-CoV-2 Spike Modulates Viral Sensitivity to Type I Interferon and IFITM2 (Q107473264) (← links)
- Why All the Fury over Furin? (Q107982009) (← links)
- Mechanical activation of spike fosters SARS-CoV-2 viral infection (Q108393051) (← links)
- Genome-wide CRISPR activation screen identifies candidate receptors for SARS-CoV-2 entry (Q108396416) (← links)
- Systematic analysis of SARS-CoV-2 infection of an ACE2-negative human airway cell (Q108396431) (← links)
- Cellular host factors for SARS-CoV-2 infection (Q108396446) (← links)
- CD209L/L-SIGN and CD209/DC-SIGN Act as Receptors for SARS-CoV-2 (Q108396536) (← links)
- Interactions of SARS-CoV-2 with the Blood–Brain Barrier (Q108503339) (← links)
- Hypoxia reduces cell attachment of SARS-CoV-2 spike protein by modulating the expression of ACE2, neuropilin-1, syndecan-1 and cellular heparan sulfate (Q108504474) (← links)
- SARS-CoV-2 S glycoprotein binding to multiple host receptors enables cell entry and infection (Q108685317) (← links)
- The SARS-CoV-2 main protease Mpro causes microvascular brain pathology by cleaving NEMO in brain endothelial cells (Q109296743) (← links)
- Furin cleavage of the SARS-CoV-2 spike is modulated by O-glycosylation (Q109649855) (← links)
- Identification of Cellular Factors Required for SARS-CoV-2 Replication (Q109919099) (← links)
- Mechanisms of SARS-CoV-2 entry into cells (Q109919182) (← links)
- Receptome profiling identifies KREMEN1 and ASGR1 as alternative functional receptors of SARS-CoV-2 (Q109919888) (← links)
- Mechanisms of Immunothrombosis by SARS-CoV-2 (Q109919934) (← links)
- SARS-CoV-2 infection triggers profibrotic macrophage responses and lung fibrosis (Q110176222) (← links)
- SARS-CoV-2 uses metabotropic glutamate receptor subtype 2 as an internalization factor to infect cells (Q110178920) (← links)
- ACE2-Independent Interaction of SARS-CoV-2 Spike Protein with Human Epithelial Cells Is Inhibited by Unfractionated Heparin (Q110245632) (← links)
- L-SIGN is a receptor on liver sinusoidal endothelial cells for SARS-CoV-2 virus (Q110457422) (← links)
- Extracellular Vimentin as a Target Against SARS‐CoV‐2 Host Cell Invasion (Q110733604) (← links)
- Heparan Sulfate Proteoglycans in Viral Infection and Treatment: A Special Focus on SARS-CoV-2 (Q110734092) (← links)
- Strikingly Different Roles of SARS-CoV-2 Fusion Peptides Uncovered by Neutron Scattering (Q110951345) (← links)
- Integrin activation is an essential component of SARS-CoV-2 infection (Q110951947) (← links)
- Role of host factors in SARS-CoV-2 entry (Q110951951) (← links)
- Neuropilin‐1‐Mediated SARS‐CoV‐2 Infection in Bone Marrow‐Derived Macrophages Inhibits Osteoclast Differentiation (Q111019276) (← links)
- The SARS-CoV-2 Spike protein disrupts human cardiac pericytes function through CD147 receptor-mediated signalling: a potential non-infective mechanism of COVID-19 microvascular disease (Q111271211) (← links)
- The spike protein of SARS-CoV-2 induces endothelial inflammation through integrin α5β1 and NF-κB signaling (Q111271260) (← links)
- SARS-CoV-2 spike engagement of ACE2 primes S2' site cleavage and fusion initiation (Q111271409) (← links)
- SARS-CoV-2: Receptor and Co-receptor Tropism Probability (Q111291435) (← links)
- Structure-function relations of the SARS-CoV-2 spike protein and impact of mutations in the variants of concern (Q111368077) (← links)
- SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels (Q131598664) (← links)
- SARS-CoV-2 replicates and displays oncolytic properties in clear cell and papillary renal cell carcinoma (Q131604200) (← links)
- SARS-CoV-2 infection as a potential risk factor for the development of cancer (Q131604205) (← links)
- Long-COVID cognitive impairments and reproductive hormone deficits in men may stem from GnRH neuronal death (Q131605107) (← links)