Evidence map›Paper›PMID 33495460›Full record

ArticleNature communications2021

Caveolae-mediated Tie2 signaling contributes to CCM pathogenesis in a brain endothelial cell-specific Pdcd10-deficient mouse model.

Huanjiao Jenny Zhou, Lingfeng Qin, Quan Jiang, Katie N Murray, Haifeng Zhang, Busu Li, Qun Lin, Morven Graham, Xinran Liu, Jaime Grutzendler and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 50 citations in OpenAlex.

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  18. Physiological functions of caveolae in endothelium.Current opinion in physiology · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Huanjiao Jenny ZhouInterdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, New Haven, CT, USA. huanjiao.zhou@yale.edu.ORCID http://orcid.org/0000-0003-3071-9473
Lingfeng Qin *Interdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.
Quan Jiang *Interdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.ORCID http://orcid.org/0000-0001-8201-6417
Katie N Murray *Department of Neurobiology, Yale University School of Medicine, New Haven, CT, USA.
Haifeng Zhang *Interdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.
Busu LiInterdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.
Qun LinInterdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.
Morven GrahamDepartment of Cell Biology, Yale University School of Medicine, New Haven, CT, USA.ORCID http://orcid.org/0000-0002-4375-3198
Xinran LiuDepartment of Cell Biology, Yale University School of Medicine, New Haven, CT, USA.
Jaime GrutzendlerDepartment of Neurobiology, Yale University School of Medicine, New Haven, CT, USA.ORCID http://orcid.org/0000-0002-5000-243X
Wang MinInterdepartmental Program in Vascular Biology and Therapeutics, Department of Pathology, Yale University School of Medicine, New Haven, CT, USA. mike.wang388@gmail.com.ORCID http://orcid.org/0000-0002-2479-6096
Yale University · US

Funding

Investigating the intracellular vesicle-mediated mechanism contributing to cerebral cavernous malformationR01HL157019 · NHLBI · YALE UNIVERSITY · PI ZHOU, JENNY HUANJIAO · 2021 to 2025
$2.1M
CCM3-mediated exocytosis in pathogenesis of cerebral cavernous malformationR01HL136507 · NHLBI · YALE UNIVERSITY · PI STERN, DAVID F · 2017 to 2020
$1.9M
Investigating cellular function and biochemical mechanism for STK24-CCM3 complexR01GM109487 · NIGMS · YALE UNIVERSITY · PI BOGGON, TITUS JONATHON, WU, DIANQING · 2014 to 2017
$1.3M
NHLBI NIH HHS R01 HL136507NHLBI NIH HHS R01 HL157019NIGMS NIH HHS R01 GM109487
6 · The paper itself

Abstract

Cerebral cavernous malformations (CCMs) are vascular abnormalities that primarily occur in adulthood and cause cerebral hemorrhage, stroke, and seizures. CCMs are thought to be initiated by endothelial cell (EC) loss of any one of the three Ccm genes: CCM1 (KRIT1), CCM2 (OSM), or CCM3 (PDCD10). Here we report that mice with a brain EC-specific deletion of Pdcd10 (Pdcd10

Indexed as

Disease Models, AnimalAnimalsApoptosis Regulatory ProteinsBrainCaveolaeCells, CulturedEndothelial CellsHemangioma, Cavernous, Central Nervous SystemHumansMiceMice, KnockoutMice, TransgenicMicroscopy, Electron, TransmissionPericytesReceptor, TIE-2Signal TransductionApoptosis Regulatory ProteinsPDCD10 protein, mouseReceptor, TIE-2Tek protein, mouse

Identifiers

PMID33495460
PMCPMC7835246
OpenAlexW3123923504

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.