Evidence map›Paper›PMID 26519113›Full record

ReviewSeminars in cell & developmental biology2015

Calcium signaling in membrane repair.

Xiping Cheng, Xiaoli Zhang, Lu Yu, Haoxing Xu

Abstract readReview
In one paragraph

Review in Seminars in cell & developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
5.9field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 97 citations in OpenAlex.

  1. Orai1 is required for CabioRxiv : the preprint server for biology · 2026
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  4. ESCRT-III function in membrane fission and repair.Nature reviews. Molecular cell biology · 2026
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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

4 authors at 1 institution in 1 country.

Xiping ChengDepartment of Molecular, Cellular, and Developmental Biology, University of Michigan, 3089 Natural Science Building (Kraus), 830 North University, Ann Arbor, MI 48109, USA. Electronic address: xiping.cheng@regeneron.com.
Xiaoli ZhangDepartment of Molecular, Cellular, and Developmental Biology, University of Michigan, 3089 Natural Science Building (Kraus), 830 North University, Ann Arbor, MI 48109, USA.
Lu YuDepartment of Molecular, Cellular, and Developmental Biology, University of Michigan, 3089 Natural Science Building (Kraus), 830 North University, Ann Arbor, MI 48109, USA.
Haoxing XuDepartment of Molecular, Cellular, and Developmental Biology, University of Michigan, 3089 Natural Science Building (Kraus), 830 North University, Ann Arbor, MI 48109, USA. Electronic address: haoxingx@umich.edu.
University of Michigan–Ann Arbor · US

Funding

The Mucolipin TRP Ion ChannelsR01NS062792 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI XU, HAOXING · 2009 to 2018
$3.3M
TRP Ca2+ Channels in the SkinR01AR060837 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI XU, HAOXING · 2012 to 2016
$1.7M
Vesicular Ca2+ Channels in Sarcolemma Repair and Muscular DystrophyR21NS091928 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI XU, HAOXING · 2015 to 2016
$414k
NIAMS NIH HHS AR060837NIAMS NIH HHS R01 AR060837NINDS NIH HHS NS062792NINDS NIH HHS NS091928NINDS NIH HHS R01 NS062792NINDS NIH HHS R21 NS091928
6 · The paper itself

Abstract

Resealing allows cells to mend damaged membranes rapidly when plasma membrane (PM) disruptions occur. Models of PM repair mechanisms include the "lipid-patch", "endocytic removal", and "macro-vesicle shedding" models, all of which postulate a dependence on local increases in intracellular Ca(2+) at injury sites. Multiple calcium sensors, including synaptotagmin (Syt) VII, dysferlin, and apoptosis-linked gene-2 (ALG-2), are involved in PM resealing, suggesting that Ca(2+) may regulate multiple steps of the repair process. Although earlier studies focused exclusively on external Ca(2+), recent studies suggest that Ca(2+) release from intracellular stores may also be important for PM resealing. Hence, depending on injury size and the type of injury, multiple sources of Ca(2+) may be recruited to trigger and orchestrate repair processes. In this review, we discuss the mechanisms by which the resealing process is promoted by vesicular Ca(2+) channels and Ca(2+) sensors that accumulate at damage sites.

Indexed as

Calcium SignalingAnimalsCell MembraneExocytosisHumansLysosomesTransient Receptor Potential ChannelsWound HealingTransient Receptor Potential ChannelsCa(2+)Calcium sensorLysosomal exocytosisMembrane repairTRPML1

Identifiers

PMID26519113
PMCPMC4681278
OpenAlexW1855156147

What OpenQuestion holds

Textmetadata
LicenceTDM
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.