Targeted protein degradation

Youguang Wang, Zihao He, Na Yin, Min Peng

Abstract read

In one paragraph

Article in hLife, 2026. 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

–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

0 citing papers in PubMed.

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.

Youguang WangState Key Laboratory of Molecular Oncology, Tsinghua University, Beijing, China.

Zihao HeState Key Laboratory of Molecular Oncology, Tsinghua University, Beijing, China.

Na YinState Key Laboratory of Molecular Oncology, Tsinghua University, Beijing, China.

Min PengState Key Laboratory of Molecular Oncology, Tsinghua University, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeted protein degradation (TPD) holds significant therapeutic potential over conventional biologics. However, existing platforms are constrained by their reliance on host protein degradation machinery and limited durability, rendering them inadequate for chronic diseases requiring sustained treatment. Here, we constructed a chimeric antigen receptor (CAR) incorporating the TNFR1 ectodomain as the antigen-binding domain (TNFR1T cells) and used CRISPR-mediated knockout of BCOR and ZC3H12A to generate persistent TNFR1T

Indexed as

BCORchimeric antigen receptor (CAR)-T cellsrheumatoid arthritissoluble antigen endocytosistargeted protein degradation (TPD)ZC3H12A

Identifiers

PMID42903904

DOI10.1016/j.hlife.2026.05.003

PMCPMC13681536

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.