Evidence map›Paper›PMID 32432944›Full record

ArticleMolecular biology of the cell2020

Flightless anchors IQGAP1 and R-ras to mediate cell extension formation and matrix remodeling.

P D Arora, K Nakajima, A Nanda, A Plaha, A Wilde, D B Sacks, C A McCulloch

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2020. 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
1.4field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  4. mSphere · 2024
    Article
  5. Article
  6. Human dermal fibroblast-derived secretory proteins for regulating nerve restoration: A bioinformatic approach.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024
    Article
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  10. Review
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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

7 authors at 2 institutions in 2 countries.

P D AroraFaculty of Dentistry, University of Toronto, Toronto, ON M5G 1G6, Canada.
K NakajimaFaculty of Dentistry, University of Toronto, Toronto, ON M5G 1G6, Canada.
A NandaFaculty of Dentistry, University of Toronto, Toronto, ON M5G 1G6, Canada.
A PlahaFaculty of Dentistry, University of Toronto, Toronto, ON M5G 1G6, Canada.
A WildeDepartments of Medical Genetics and Biochemistry, Faculty of Medicine, University of Toronto, Toronto, ON M5G 1L7, Canada.
D B SacksDepartment of Laboratory Medicine, National Institutes of Health, Bethesda, MD 20892.
C A McCullochFaculty of Dentistry, University of Toronto, Toronto, ON M5G 1G6, Canada.
University of Toronto · CANational Institutes of Health · US

Funding

IQGAP1 in tumorigenesisZIACL080017 · CLC · CLINICAL CENTER · PI SACKS, DAVID · 2012 to 2025
$0k
CIHR MOP-36332
6 · The paper itself

Abstract

Tractional remodeling of collagen fibrils by fibroblasts requires long cell extensions that mediate fibril alignment. The formation of these cell extensions involves flightless I (FliI), an actin-binding protein that contains a leucine-rich-repeat (LRR), which binds R-ras and may regulate cdc42. We considered that FliI interacts with small GTPases and their regulators to mediate assembly of cell extensions. Mass spectrometry analyses of FliI immunoprecipitates showed abundant Ras GTPase-activating-like protein (IQGAP1), which in immunostained samples colocalized with FliI at cell adhesions. Knockdown of IQGAP1 reduced the numbers of cell extensions and the alignment of collagen fibrils. In experiments using dominant negative mutants, cdc42 activity was required for the formation of short extensions while R-ras was required for the formation of long extensions. Immunoprecipitation of wild-type and mutant constructs showed that IQGAP1 associated with cdc42 and R-ras; this association required the GAP-related domain (1004-1237 aa) of IQGAP1. In cells transfected with FliI mutants, the LRR of FliI, but not its gelsolin-like domains, mediated association with cdc42, R-ras, and IQGAP1. We conclude that FliI interacts with IQGAP1 and co-ordinates with cdc42 and R-ras to control the formation of cell extensions that enable collagen tractional remodeling.

Indexed as

3T3 CellsAnimalscdc42 GTP-Binding ProteinCell AdhesionCell Surface ExtensionsCollagenExtracellular MatrixMiceMicrofilament ProteinsModels, BiologicalProtein BindingProtein Domainsras GTPase-Activating Proteinsras ProteinsTrans-Activatorscdc42 GTP-Binding ProteinCollagenFlII protein, mouseIQ motif containing GTPase activating protein 1Microfilament Proteinsras GTPase-Activating Proteinsras ProteinsRras protein, mouseTrans-Activators

Identifiers

PMID32432944
PMCPMC7521798
OpenAlexW3028125815

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.