Evidence map›Paper›PMID 39288219›Full record

ReviewScience signaling2024

The role of signaling pathways mediated by the GPCRs CysLTR1/2 in melanocyte proliferation and senescence.

Thomas Huber, Mizuho Horioka-Duplix, Yuanhuang Chen, Victoria R Saca, Emilie Ceraudo, Yu Chen, Thomas P Sakmar

Abstract readReview
In one paragraph

Review in Science signaling, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Cutaneous Melanoma in the Context of Aging.Medicina (Kaunas, Lithuania) · 2025
    Review
  3. The mutual interaction of TRPC5 channel with polycystin proteins.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    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

7 authors.

Thomas HuberLaboratory of Chemical Biology and Signal Transduction, Rockefeller University, New York, NY 10065, USA.ORCID 0000-0002-1844-262X
Mizuho Horioka-DuplixLaboratory of Chemical Biology and Signal Transduction, Rockefeller University, New York, NY 10065, USA.
Yuanhuang ChenLaboratory of Chemical Biology and Signal Transduction, Rockefeller University, New York, NY 10065, USA.ORCID 0000-0001-7404-5170
Victoria R SacaLaboratory of Chemical Biology and Signal Transduction, Rockefeller University, New York, NY 10065, USA.ORCID 0000-0003-3418-4525
Emilie CeraudoLaboratory of Chemical Biology and Signal Transduction, Rockefeller University, New York, NY 10065, USA.ORCID 0000-0001-6563-9751
Yu ChenHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.ORCID 0000-0002-0171-3884
Thomas P SakmarLaboratory of Chemical Biology and Signal Transduction, Rockefeller University, New York, NY 10065, USA.ORCID 0000-0002-2836-8953

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
SPORE In Prostate CancerP50CA092629 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI David B. Solit · 2001 to 2026
$63.0M
Role of ETS factors in specifying prostate luminal cell identity and androgen receptor dependenceR01CA193837 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI SAWYERS, CHARLES L. · 2015 to 2025
$4.7M
Tri-Institutional PhD Program in Chemical BiologyT32GM136640 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI DEREK S TAN · 2020 to 2026
$2.4M
Understanding the roles of TMPRSS2 and ERG in pathogenesis of prostate cancer.K08CA140946 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI CHEN, YU · 2009 to 2013
$796k
Tri-Institutional PhD Program in Chemical BiologyT32GM115327 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI TAN, DEREK S · 2015 to 2019
$741k
NCI NIH HHS K08 CA140946NCI NIH HHS P30 CA008748NCI NIH HHS P50 CA092629NCI NIH HHS R01 CA193837NIGMS NIH HHS T32 GM115327NIGMS NIH HHS T32 GM136640
6 · The paper itself

Abstract

In contrast with sun exposure-induced melanoma, rarer melanocytic tumors and neoplasms with low mutational burden present opportunities to study isolated signaling mechanisms. These include uveal melanoma and blue nevi, which are often driven by mutations within the G protein-coupled signaling cascade downstream of cysteinyl leukotriene receptor 2. Here, we review how the same mutations within this pathway drive the growth of melanocytes in one tissue but can inhibit the growth of those in another, exemplifying the role of the tissue environment in the delicate balance between uncontrolled cell growth and senescence.

Indexed as

Cell ProliferationCellular SenescenceMelanocytesReceptors, LeukotrieneSignal TransductionAnimalsHumansMelanomaMutationReceptors, G-Protein-CoupledUveal MelanomaUveal Neoplasmscysteinyl leukotriene receptor 2leukotriene D4 receptorReceptors, G-Protein-CoupledReceptors, Leukotriene

Identifiers

PMID39288219
PMCPMC11920964

What OpenQuestion holds

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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.