Evidence map›Paper›PMID 35000542›Full record

ReviewAutophagy2023

The exploitation of host autophagy and ubiquitin machinery by

Mohd Shariq, Neha Quadir, Anwar Alam, Sheeba Zarin, Javaid A Sheikh, Neha Sharma, Jasmine Samal, Uzair Ahmad, Indu Kumari, Seyed E Hasnain and 1 more

Open access · greenAbstract readReview
In one paragraph

Review in Autophagy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
14.2field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. Review
  3. Inhalational therapy of pulmonary infectionActa pharmaceutica Sinica. B · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Drug resistance mechanisms inFrontiers in pharmacology · 2026
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. SMURF2 inhibits autophagic control ofbioRxiv : the preprint server for biology · 2025
    Article
  14. Article
  15. Autophagy in Acute Lung Injury.Cell biochemistry and biophysics · 2025
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

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

11 authors at 5 institutions in 1 country.

Mohd ShariqInflammation Biology and Cell Signaling Laboratory, National Institute of Pathology-ICMR, Ansari Nagar West, New Delhi, India.
Neha QuadirInflammation Biology and Cell Signaling Laboratory, National Institute of Pathology-ICMR, Ansari Nagar West, New Delhi, India.
Anwar AlamInflammation Biology and Cell Signaling Laboratory, National Institute of Pathology-ICMR, Ansari Nagar West, New Delhi, India.
Sheeba ZarinInflammation Biology and Cell Signaling Laboratory, National Institute of Pathology-ICMR, Ansari Nagar West, New Delhi, India.
Javaid A SheikhDepartment of Biotechnology, School of Chemical and Life Sciences, Jamia Hamdard, New Delhi, India.
Neha SharmaInflammation Biology and Cell Signaling Laboratory, National Institute of Pathology-ICMR, Ansari Nagar West, New Delhi, India.
Jasmine SamalInflammation Biology and Cell Signaling Laboratory, National Institute of Pathology-ICMR, Ansari Nagar West, New Delhi, India.
Uzair AhmadInflammation Biology and Cell Signaling Laboratory, National Institute of Pathology-ICMR, Ansari Nagar West, New Delhi, India.
Indu KumariInflammation Biology and Cell Signaling Laboratory, National Institute of Pathology-ICMR, Ansari Nagar West, New Delhi, India.
Seyed E HasnainDepartment of Biochemical Engineering and Biotechnology, Indian Institute of Technology, Delhi (IIT-D), New Delhi, India.
Nasreen Z EhteshamInflammation Biology and Cell Signaling Laboratory, National Institute of Pathology-ICMR, Ansari Nagar West, New Delhi, India.
National Institute of Pathology · INInstitute of Molecular Medicine · INDepartment of Biotechnology · INIndian Institute of Technology Delhi · INJamia Hamdard · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intracellular pathogens have evolved various efficient molecular armaments to subvert innate defenses. Cellular ubiquitination, a normal physiological process to maintain homeostasis, is emerging one such exploited mechanism. Ubiquitin (Ub), a small protein modifier, is conjugated to diverse protein substrates to regulate many functions. Structurally diverse linkages of poly-Ub to target proteins allow enormous functional diversity with specificity being governed by evolutionarily conserved enzymes (E3-Ub ligases). The Ub-binding domain (UBD) and LC3-interacting region (LIR) are critical features of macroautophagy/autophagy receptors that recognize Ub-conjugated on protein substrates. Emerging evidence suggests that E3-Ub ligases unexpectedly protect against intracellular pathogens by tagging poly-Ub on their surfaces and targeting them to phagophores. Two E3-Ub ligases, PRKN and SMURF1, provide immunity against

Indexed as

Mycobacterium tuberculosisUbiquitinAutophagyCarrier ProteinsImmunityUbiquitin-Protein LigasesCarrier ProteinsUbiquitinUbiquitin-Protein LigasesAutophagyE3-Ub ligaseintracellular pathogensLC3phagolysosomeubiquitin-binding receptorsvirulence effectorsxenophagy

Identifiers

PMID35000542
PMCPMC9809970
OpenAlexW4206349297

What OpenQuestion holds

Textmetadata
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.