Evidence map›Paper›PMID 30975920›Full record

ArticleJournal of cell science2019

A unique role for clathrin light chain A in cell spreading and migration.

Oxana M Tsygankova, James H Keen

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Clathrin Light Chains: Not to Be Taken so Lightly.Frontiers in cell and developmental biology · 2021
    Review
  12. Clathrin light chain diversity regulates membrane deformation in vitro and synaptic vesicle formation in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  13. Article
  14. Article
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

2 authors at 1 institution in 1 country.

Oxana M TsygankovaDepartment of Biochemistry and Molecular Biology, Cell Biology and Signaling Program of the Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA.
James H KeenDepartment of Biochemistry and Molecular Biology, Cell Biology and Signaling Program of the Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA James.keen@jefferson.edu.ORCID 0000-0003-0753-8690
Thomas Jefferson University · US

Funding

X-Ray Crystallography and Macromolecular CharacterizationP30CA056036 · NCI · THOMAS JEFFERSON UNIVERSITY · PI Andrew Chapman · 1995 to 2026
$94.8M
Regulation of Clathrin and Adaptor FunctionR01GM049217 · NIGMS · THOMAS JEFFERSON UNIVERSITY · PI KEEN, JAMES H · 1994 to 2016
$3.8M
NCI NIH HHS P30 CA056036NIGMS NIH HHS R01 GM049217
6 · The paper itself

Abstract

Clathrin heavy chain is the structural component of the clathrin triskelion, but unique functions for the two distinct and highly conserved clathrin light chains (CLCa and CLCb, also known as CLTA and CLTB, respectively) have been elusive. Here, we show that following detachment and replating, CLCa is uniquely responsible for promoting efficient cell spreading and migration. Selective depletion of CLCa, but not of CLCb, reduced the initial phase of isotropic spreading of HeLa, H1299 and HEK293 cells by 60-80% compared to siRNA controls, and wound closure and motility by ∼50%. Surface levels of β1-integrins were unaffected by CLCa depletion. However, CLCa was required for effective targeting of FAK (also known as PTK2) and paxillin to the adherent surface of spreading cells, for integrin-mediated activation of Src, FAK and paxillin, and for maturation of focal adhesions, but not their microtubule-based turnover. Depletion of CLCa also blocked the interaction of clathrin with the nucleation-promoting factor WAVE complex, and altered actin distribution. Furthermore, preferential recruitment of CLCa to budding protrusions was also observed. These results comprise the first identification of CLCa-specific functions, with implications for normal and neoplastic integrin-based signaling and cell migration.

Indexed as

Cell Line, TumorCell MovementClathrin Light ChainsFocal AdhesionsHumansSignal TransductionClathrin Light ChainsCell spreadingClathrinFocal adhesionsIntegrin signaling

Identifiers

PMID30975920
PMCPMC6550010
OpenAlexW2937741430

What OpenQuestion holds

Textmetadata
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.