Evidence map›Paper›PMID 42541411›Full record

ArticleFEBS letters2026

An epithelial GPR35 isoform supports tumor-associated transcriptional and metabolic phenotypes.

Jørgen D Rønneberg, Martine Hjeltnes, Josephine Krieger, Joshua E Elias, Maria Stensland, Kristian Holm, Xiaojun Jiang, Chuki Khangsar, Tuula A Nyman, Arthur Kaser and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FEBS letters, 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

15 authors.

Jørgen D RønnebergDivision of Surgery and Specialized Medicine, Norwegian PSC Research Center, Oslo University Hospital Rikshospitalet, Norway.
Martine HjeltnesDivision of Surgery and Specialized Medicine, Norwegian PSC Research Center, Oslo University Hospital Rikshospitalet, Norway.
Josephine KriegerDivision of Surgery and Specialized Medicine, Norwegian PSC Research Center, Oslo University Hospital Rikshospitalet, Norway.
Joshua E EliasCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, UK.
Maria StenslandDepartment of Immunology, University of Oslo and Oslo University Hospital, Norway.
Kristian HolmDivision of Surgery and Specialized Medicine, Norwegian PSC Research Center, Oslo University Hospital Rikshospitalet, Norway.
Xiaojun JiangDivision of Surgery and Specialized Medicine, Norwegian PSC Research Center, Oslo University Hospital Rikshospitalet, Norway.
Chuki KhangsarDivision of Surgery and Specialized Medicine, Norwegian PSC Research Center, Oslo University Hospital Rikshospitalet, Norway.
Tuula A NymanDepartment of Immunology, University of Oslo and Oslo University Hospital, Norway.
Arthur KaserCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, UK.
Johannes R HovDivision of Surgery and Specialized Medicine, Norwegian PSC Research Center, Oslo University Hospital Rikshospitalet, Norway.
Tom H KarlsenDivision of Surgery and Specialized Medicine, Norwegian PSC Research Center, Oslo University Hospital Rikshospitalet, Norway.
Nicole C KaneiderCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, UK.
Frode L JahnsenDepartment of Pathology, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Norway.
Georg SchneditzDivision of Surgery and Specialized Medicine, Norwegian PSC Research Center, Oslo University Hospital Rikshospitalet, Norway.ORCID https://orcid.org/0000-0001-6734-5861

Funding

Leona M. and Harry B. Helmsley Charitable Trust G-2408-07256Norwegian PSC Research CenterPSC Partners Seeking a CureSouth-Eastern Norway Regional Health Authority (Helse Sør-Øst RHF)UiO:Livsvitenskap, Universitetet i Oslo
6 · The paper itself

Abstract

G protein-coupled receptor 35 (GPR35) has been implicated in cancer, but the functional roles of its isoforms remain unresolved. Here, we characterize GPR35-long, an N-terminally extended epithelial isoform selectively enriched in colorectal cancer and cholangiocarcinoma. Mass spectrometry and immunohistochemistry confirmed GPR35-long protein expression in tumor cells. Functional analyses revealed that GPR35-long supports tumor-associated transcriptional programs, enhances cellular ATP production, and exhibits increased constitutive and ligand-induced beta-arrestin signaling. These phenotypes were selectively suppressed by the inverse agonist CID-2745687, identifying GPR35-long as a functionally distinct isoform with selective pharmacological sensitivity in tumor cells.

Indexed as

CholangiocarcinomaColorectal NeoplasmsReceptors, G-Protein-CoupledTranscription, GeneticAdenosine TriphosphateAnimalsbeta-ArrestinsCell Line, TumorGene Expression Regulation, NeoplasticHumansPhenotypeProtein IsoformsSignal TransductionAdenosine Triphosphatebeta-ArrestinsGPR35 protein, humanProtein IsoformsReceptors, G-Protein-Coupledcell metabolismcell signalingcolon cancerG protein‐coupled receptormolecular pharmacology

Identifiers

PMID42541411
PMCPMC13656332

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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.