Evidence map›Paper›PMID 34359983›Full record

ArticleCells2021

SARS-CoV-2 Cellular Entry Is Independent of the ACE2 Cytoplasmic Domain Signaling.

Thankamani Karthika, Jeswin Joseph, V R Akshay Das, Niranjana Nair, Packirisamy Charulekha, Melvin Daniel Roji, V Stalin Raj

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
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  7. Facilitating and restraining virus infection using cell-attachable soluble viral receptors.Proceedings of the National Academy of Sciences of the United States of America · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Thankamani KarthikaVirology Scientific Research (VSR) Laboratory, School of Biology, Indian Institute of Science Education and Research Thiruvananthapuram, Kerala 695551, India.ORCID 0000-0002-9100-4466
Jeswin JosephVirology Scientific Research (VSR) Laboratory, School of Biology, Indian Institute of Science Education and Research Thiruvananthapuram, Kerala 695551, India.ORCID 0000-0002-5371-2779
V R Akshay DasVirology Scientific Research (VSR) Laboratory, School of Biology, Indian Institute of Science Education and Research Thiruvananthapuram, Kerala 695551, India.ORCID 0000-0001-9377-5881
Niranjana NairVirology Scientific Research (VSR) Laboratory, School of Biology, Indian Institute of Science Education and Research Thiruvananthapuram, Kerala 695551, India.ORCID 0000-0003-3374-3321
Packirisamy CharulekhaVirology Scientific Research (VSR) Laboratory, School of Biology, Indian Institute of Science Education and Research Thiruvananthapuram, Kerala 695551, India.ORCID 0000-0003-3620-8113
Melvin Daniel RojiVirology Scientific Research (VSR) Laboratory, School of Biology, Indian Institute of Science Education and Research Thiruvananthapuram, Kerala 695551, India.ORCID 0000-0002-1219-4987
V Stalin RajVirology Scientific Research (VSR) Laboratory, School of Biology, Indian Institute of Science Education and Research Thiruvananthapuram, Kerala 695551, India.ORCID 0000-0003-2250-8481
Indian Institute of Science Education and Research Thiruvananthapuram · IN

Funding

Science and Engineering Research Board IPA/2020/000070
6 · The paper itself

Abstract

Recently emerged severe acute respiratory syndrome coronavirus (SARS-CoV)-1 and -2 initiate virus infection by binding of their spike glycoprotein with the cell-surface receptor angiotensin-converting enzyme 2 (ACE2) and enter into the host cells mainly via the clathrin-mediated endocytosis pathway. However, the internalization process post attachment with the receptor is not clear for both SARS-CoV-1 and -2. Understanding the cellular factor/s or pathways used by these CoVs for internalization might provide insights into viral pathogenesis, transmission, and development of novel therapeutics. Here, we demonstrated that the cytoplasmic tail of ACE2 is not essential for the entry of SARS-CoV-1 and -2 by using bioinformatics, mutational, confocal imaging, and pseudotyped SARS-CoVs infection studies. ACE2 cytoplasmic domain (cytACE2) contains a conserved internalization motif and eight putative phosphorylation sites. Complete cytoplasmic domain deleted ACE2 (∆cytACE2) was properly synthesized and presented on the surface of HEK293T and BHK21 cells like wtACE2. The SARS-CoVs S1 or RBD of spike protein binds and colocalizes with the receptors followed by internalization into the host cells. Moreover, pseudotyped SARS-CoVs entered into wtACE2- and ∆cytACE2-transfected cells but not into dipeptidyl peptidase 4 (DPP4)-expressing cells. Their entry was significantly inhibited by treatment with dynasore, a dynamin inhibitor, and NH

Indexed as

Signal TransductionVirus InternalizationAngiotensin-Converting Enzyme 2AnimalsChlorocebus aethiopsCOVID-19HEK293 CellsHumansProtein DomainsSARS-CoV-2Vero CellsACE2 protein, humanAngiotensin-Converting Enzyme 2ACE2ACE2 internalizationcoronavirus entrySARS-CoV-1SARS-CoV-2

Identifiers

PMID34359983
PMCPMC8304749
OpenAlexW3185950833

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.