Evidence map›Paper›PMID 35891784›Full record

ReviewComputational and structural biotechnology journal2022

Crystallographic mining of ASK1 regulators to unravel the intricate PPI interfaces for the discovery of small molecule.

Ashish Kumar Agrahari, Madhu Dikshit, Shailendra Asthana

Abstract readReview
In one paragraph

Review in Computational and structural biotechnology journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. SSTNSignal transduction and targeted therapy · 2026
    Article
  2. The GATA3-RFPL3-ASK1 axis suppresses breast cancer growth and lung metastasis.Apoptosis : an international journal on programmed cell death · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. PGAM5 Modulates Macrophage Polarization, Aggravating Inflammation in COPD via the NF-κB Pathway.International journal of chronic obstructive pulmonary disease · 2025
    Article
  8. Review
  9. The Function of ASK1 in Sepsis and Stress-Induced Disorders.International journal of molecular sciences · 2023
    Review
  10. Article
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

3 authors.

Ashish Kumar AgrahariTranslational Health Science and Technology Institute (THSTI), Faridabad, Haryana, India.
Madhu DikshitTranslational Health Science and Technology Institute (THSTI), Faridabad, Haryana, India.
Shailendra AsthanaTranslational Health Science and Technology Institute (THSTI), Faridabad, Haryana, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein seldom performs biological activities in isolation. Understanding the protein-protein interactions' physical rewiring in response to pathological conditions or pathogen infection can help advance our comprehension of disease etiology, progression, and pathogenesis, which allow us to explore the alternate route to control the regulation of key target interactions, timely and effectively. Nonalcoholic steatohepatitis (NASH) is now a global public health problem exacerbated due to the lack of appropriate treatments. The most advanced anti-NASH lead compound (selonsertib) is withdrawn, though it is able to inhibit its target Apoptosis signal-regulating kinase 1 (ASK1) completely, indicating the necessity to explore alternate routes rather than complete inhibition. Understanding the interaction fingerprints of endogenous regulators at the molecular level that underpin disease formation and progression may spur the rationale of designing therapeutic strategies. Based on our analysis and thorough literature survey of the various key regulators and PTMs, the current review emphasizes PPI-based drug discovery's relevance for NASH conditions. The lack of structural detail (interface sites) of ASK1 and its regulators makes it challenging to characterize the PPI interfaces. This review summarizes key regulators interaction fingerprinting of ASK1, which can be explored further to restore the homeostasis from its hyperactive states for therapeutics intervention against NASH.

Indexed as

ASK1ASK1, Apoptosis signal-regulating kinase 1CFLAR, CASP8 and FADD-like apoptosis regulatorCREG, Cellular repressor of E1A-stimulated genesDKK3, Dickkopf-related protein 3Interaction fingerprintNAFLD, Non-alcoholic fatty liver diseaseNASHNASH, Nonalcoholic steatohepatitisPPI, Protein-protein interactionProtein-protein interactionPTM, Post-trancriptional modificationPTMsTNFAIP3, TNF Alpha Induced Protein 3TRAF2/6, Tumor necrosis factor receptor (TNFR)-associated factor2/6TRIM48, Tripartite Motif Containing 48TRX, ThioredoxinUSP9X, Ubiquitin Specific Peptidase 9 X-Linked

Identifiers

PMID35891784
PMCPMC9294202

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.