Evidence map›Paper›PMID 34829931›Full record

ReviewBiomedicines2021

Posttranslational Modifications in PD-L1 Turnover and Function: From Cradle to Grave.

Xinfang Yu, Wei Li, Ken H Young, Yong Li

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

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  11. ID3 enhances PD-L1 expression by restructuring MYC to promote colorectal cancer immune evasion.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

4 authors at 2 institutions in 1 country.

Xinfang YuSection of Epidemiology and Population Science, Department of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Wei LiSection of Epidemiology and Population Science, Department of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Ken H YoungHematopathology Division, Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA.
Yong LiSection of Epidemiology and Population Science, Department of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.ORCID 0000-0001-8838-1714
Baylor College of Medicine · USDuke Medical Center · US

Funding

Cancer Prevention and Research Institute of Texas RR190043
6 · The paper itself

Abstract

Programmed death-ligand 1 (PD-L1) is one of the most classic immune checkpoint molecules. Cancer cells express PD-L1 to inhibit the activity of effector T cells' cytotoxicity through programmed death 1 (PD-1) engagement in exposure to inflammatory cytokines. PD-L1 expression levels on cancer cells might affect the clinical response to anti-PD-1/PD-L1 therapies. Hence, understanding molecular mechanisms for regulating PD-L1 expression is essential for improving the clinical response rate and efficacy of PD-1/PD-L1 blockade. Posttranslational modifications (PTMs), including phosphorylation, glycosylation, ubiquitination, and acetylation, regulate PD-L1 stability, cellular translocation, and interaction with its receptor. A coordinated positive and negative regulation via PTMs is required to ensure the balance and function of the PD-L1 protein. In this review, we primarily focus on the roles of PTMs in PD-L1 expression, trafficking, and antitumor immune response. We also discuss the implication of PTMs in anti-PD-1/PD-L1 therapies.

Indexed as

immunotherapyposttranslational modificationsprogrammed death 1programmed death-ligand 1stabilitytranslocation

Identifiers

PMID34829931
PMCPMC8615371
OpenAlexW3214461828

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.