Evidence map›Paper›PMID 30727895›Full record

ArticleCurrent cancer drug targets2019

Autophagy and Apoptosis Specific Knowledgebases-guided Systems Pharmacology Drug Research.

Peihao Fan, Nanyi Wang, Lirong Wang, Xie X-Q

Open access · greenAbstract read
In one paragraph

Article in Current cancer drug targets, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

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

4 authors at 1 institution in 1 country.

Peihao FanDepartment of Pharmaceutical Sciences and Computational Chemical Genomics Screening Center, University of Pittsburgh, 3501 Terrace Street, PA, United States.
Nanyi WangSchool of Pharmacy, University of Pittsburgh, 335 Sutherland Drive, 206 Salk Pavilion, PA, United States.
Lirong WangSchool of Pharmacy, University of Pittsburgh, 335 Sutherland Drive, 206 Salk Pavilion, PA, United States.
Xie X-QSchool of Pharmacy, University of Pittsburgh, 335 Sutherland Drive, 206 Salk Pavilion, PA, United States.
University of Pittsburgh · US

Funding

NIDA Center of Excellence OF Computational Drug Abuse Research (CDAR)P30DA035778 · NIDA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BAHAR, IVET, XIE, XIANG-QUN · 2014 to 2018
$5.4M
NIDA NIH HHS P30 DA035778
6 · The paper itself

Abstract

backgroundAutophagy and apoptosis are the basic physiological processes in cells that clean up aged and mutant cellular components or even the entire cells. Both autophagy and apoptosis are disrupted in most major diseases such as cancer and neurological disorders. Recently, increasing attention has been paid to understand the crosstalk between autophagy and apoptosis due to their tightly synergetic or opposite functions in several pathological processes.

objectiveThis study aims to assist autophagy and apoptosis-related drug research, clarify the intense and complicated connections between two processes, and provide a guide for novel drug development.

methodsWe established two chemical-genomic databases which are specifically designed for autophagy and apoptosis, including autophagy- and apoptosis-related proteins, pathways and compounds. We then performed network analysis on the apoptosis- and autophagy-related proteins and investigated the full protein-protein interaction (PPI) network of these two closely connected processes for the first time.

resultsThe overlapping targets we discovered show a more intense connection with each other than other targets in the full network, indicating a better efficacy potential for drug modulation. We also found that Death-associated protein kinase 1 (DAPK1) is a critical point linking autophagy- and apoptosis-related pathways beyond the overlapping part, and this finding may reveal some delicate signaling mechanism of the process. Finally, we demonstrated how to utilize our integrated computational chemogenomics tools on in silico target identification for small molecules capable of modulating autophagy- and apoptosis-related pathways.

conclusionThe knowledge-bases for apoptosis and autophagy and the integrated tools will accelerate our work in autophagy and apoptosis-related research and can be useful sources for information searching, target prediction, and new chemical discovery.

Indexed as

ApoptosisAutophagyKnowledge BasesAntineoplastic AgentsComputational BiologyDrug DevelopmentHumansMolecular Docking SimulationNeoplasmsProtein Interaction MappingSignal TransductionAntineoplastic AgentsapoptosisAutophagycancernetwork analysisneurological diseasessystems pharmacology.

Identifiers

PMID30727895
PMCPMC6774909
OpenAlexW2914478612

What OpenQuestion holds

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LicenceTDM
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.