Evidence map›Paper›PMID 36712071›Full record

ArticlebioRxiv : the preprint server for biology2023

Enkurin: A novel marker for myeloproliferative neoplasms from platelet, megakaryocyte, and whole blood specimens.

Sumanth Mosale Seetharam, Yi Liu, Jason Wu, Lenn Fechter, Kanagavel Murugesan, Holden Maecker, Jason Gotlib, James Zehnder, Ramasamy Paulmurugan, Anandi Krishnan

Open access · greenAbstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. 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, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Sumanth Mosale SeetharamDepartment of Pathology, Stanford University, Stanford, CA.
Yi LiuDepartment of Radiology, Stanford University, Stanford, CA.
Jason WuHigh-Throughput Bioscience Center (HTBC), Stanford University School of Medicine, Stanford, CA.
Lenn FechterStanford Cancer Institute, Stanford University School of Medicine, Stanford, CA.
Kanagavel MurugesanDepartment of Pathology, Stanford University, Stanford, CA.
Holden MaeckerStanford Cancer Institute, Stanford University School of Medicine, Stanford, CA.
Jason GotlibStanford Cancer Institute, Stanford University School of Medicine, Stanford, CA.
James ZehnderDepartment of Pathology, Stanford University, Stanford, CA.
Ramasamy PaulmuruganDepartment of Radiology, Stanford University, Stanford, CA.
Anandi KrishnanDepartment of Pathology, Stanford University, Stanford, CA.
Stanford University · USHigh Throughput Biology (United States) · US

Funding

Stanford Center for Clinical & Translational Education and Research (Spectrum)UL1TR003142 · NCATS · STANFORD UNIVERSITY · PI O'HARA, RUTH M · 2019 to 2023
$45.0M
Spectrum Stanford Center for clinical and Translational Research and EducationUL1TR001085 · NCATS · STANFORD UNIVERSITY · PI CULLEN, MARK RICHARD, GREENBERG, HARRY BERNARD · 2013 to 2017
$37.1M
Integrated Clinical and Transcriptomic Profiling to Characterize Disease PhenotypeK08HG010061 · NHGRI · STANFORD UNIVERSITY · PI KRISHNAN, ANANDI · 2018 to 2022
$955k
High Throughput DNA Sequencer UpgradeS10OD018220 · OD · STANFORD UNIVERSITY · PI COLLER, JOHN · 2014 to 2014
$596k
Computer ClusterS10OD021763 · OD · STANFORD UNIVERSITY · PI JI, HANLEE P · 2016 to 2016
$481k
NCATS NIH HHS UL1 TR001085NCATS NIH HHS UL1 TR003142NHGRI NIH HHS K08 HG010061NIH HHS S10 OD018220NIH HHS S10 OD021763
6 · The paper itself

Abstract

Impaired protein homeostasis, though well established in age-related disorders, has been linked in recent research with the pathogenesis of myeloproliferative neoplasms (MPNs). As yet, however, little is known about MPN-specific modulators of proteostasis, thus impeding our ability for increased mechanistic understanding and discovery of additional therapeutic targets. Loss of proteostasis, in itself, is traced to dysregulated mechanisms in protein folding and intracellular calcium signaling at the endoplasmic reticulum (ER). Here, using VISUAL ABSTRACT: Key Points: Enkurin, a calcium adaptor protein, is identified as a novel marker of pathogenesis in MPNs.MPN megakaryocyte and platelet expression of enkurin at RNA and protein levels is inversely associated with a cell differentiation cycle gene, CDC20.Likely role for dysregulated calcium homeostasis, and ER and protein folding stress in MPN transformation.

Identifiers

PMID36712071
PMCPMC9881897
OpenAlexW4313750696

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.