Evidence map›Paper›PMID 38940198›Full record

ArticleJournal of cell science2024

TMEM16F scramblase regulates angiogenesis via endothelial intracellular signaling.

Ke Zoe Shan, Trieu Le, Pengfei Liang, Ping Dong, Augustus J Lowry, Polina Kremmyda, Lena Claesson-Welsh, Huanghe Yang

Abstract read
In one paragraph

Article in Journal of cell science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
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  3. Review
  4. A cell-based scrambling assay reveals the phospholipid headgroup preference of TMEM16F on the plasma membrane.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  7. Article
  8. Article
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  10. Review
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  13. CaInternational journal of molecular sciences · 2024
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Ke Zoe ShanDepartment of Biochemistry, Duke University, School of Medicine, Durham, NC 27710, USA.
Trieu LeDepartment of Biochemistry, Duke University, School of Medicine, Durham, NC 27710, USA.
Pengfei LiangDepartment of Biochemistry, Duke University, School of Medicine, Durham, NC 27710, USA.
Ping DongDepartment of Biochemistry, Duke University, School of Medicine, Durham, NC 27710, USA.
Augustus J LowryDepartment of Biochemistry, Duke University, School of Medicine, Durham, NC 27710, USA.
Polina KremmydaDepartment of Immunology, Genetics and Pathology, Uppsala University, Rudbeck, Beijer and SciLifeLab Laboratory, Uppsala 751 85, Sweden.
Lena Claesson-WelshDepartment of Immunology, Genetics and Pathology, Uppsala University, Rudbeck, Beijer and SciLifeLab Laboratory, Uppsala 751 85, Sweden.
Huanghe YangDepartment of Biochemistry, Duke University, School of Medicine, Durham, NC 27710, USA.ORCID 0000-0001-9521-9328

Funding

Manipulating TMEM16F lipid scramblase to understand the transbilayer phospholipid transport phenomenonDP2GM126898 · NIGMS · DUKE UNIVERSITY · PI YANG, HUANGHE · 2017 to 2017
$2.2M
Advancing mechanistic understanding of membrane ion and lipid transportR35GM153196 · NIGMS · DUKE UNIVERSITY · PI Huanghe Yang · 2024 to 2026
$1.4M
American Heart Association 20PRE35120162NIGMS NIH HHS DP2 GM126898NIGMS NIH HHS R35 GM153196NIH HHS DP2GM126898NIH HHS NIH-DP2GM126898
6 · The paper itself

Abstract

TMEM16F (also known as ANO6), a Ca2+-activated lipid scramblase (CaPLSase) that dynamically disrupts lipid asymmetry, plays a crucial role in various physiological and pathological processes, such as blood coagulation, neurodegeneration, cell-cell fusion and viral infection. However, the mechanisms through which it regulates these processes remain largely elusive. Using endothelial cell-mediated angiogenesis as a model, here we report a previously unknown intracellular signaling function of TMEM16F. We demonstrate that TMEM16F deficiency impairs developmental retinal angiogenesis in mice and disrupts angiogenic processes in vitro. Biochemical analyses indicate that the absence of TMEM16F enhances the plasma membrane association of activated Src kinase. This in turn increases VE-cadherin phosphorylation and downregulation, accompanied by suppressed angiogenesis. Our findings not only highlight the role of intracellular signaling by TMEM16F in endothelial cells but also open new avenues for exploring the regulatory mechanisms for membrane lipid asymmetry and their implications in disease pathogenesis.

Indexed as

AnoctaminsEndothelial CellsSignal TransductionAngiogenesisAnimalsAntigens, CDCadherin 5CadherinsCell MembraneHumansHuman Umbilical Vein Endothelial CellsMiceMice, Inbred C57BLMice, KnockoutNeovascularization, PhysiologicPhospholipid Transfer ProteinsANO6 protein, mouseAnoctaminsAntigens, CDCadherin 5CadherinsPhospholipid Transfer Proteinssrc-Family KinasesAngiogenesisEndothelial cellsScramblaseSrcTMEM16FVE-cadherin

Identifiers

PMID38940198
PMCPMC11273297

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.