Evidence map›Paper›PMID 19952357›Full record

ArticleJournal of leukocyte biology2010

Regulation of class A scavenger receptor-mediated cell adhesion and surface localization by PI3K: identification of a regulatory cytoplasmic motif.

Jill Cholewa, Dejan Nikolic, Steven R Post

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2010. 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
0.1field-weighted citation impact, top 49% 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, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Scavenger receptor A1 participates in uptake ofEmerging microbes & infections · 2021
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. GRP78 inhibits macrophage adhesion via SR-A.Journal of biomedical research · 2014
    Article
  10. Review
  11. Article
  12. Review
  13. 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

3 authors at 2 institutions in 1 country.

Jill CholewaGraduate Center for Nutritional Sciences, The University of Kentucky, Lexington, Kentucky, USA.
Dejan Nikolic
Steven R Post
University of Arkansas for Medical Sciences · USUniversity of Kentucky · US

Funding

TRAINING PROGRAM IN OXIDATIVE STRESS AND NUTRITIONT32DK007778 · NIDDK · UNIVERSITY OF KENTUCKY · PI WEBB, NANCY R · 2000 to 2019
$2.5M
Function and Regulation of SR-A in AtherosclerosisR01HL089588 · NHLBI · UNIV OF ARKANSAS FOR MED SCIS · PI POST, STEVEN · 2008 to 2011
$1.4M
Regulation of Ras Signaling by Rlf In HypertrophyR01HL075241 · NHLBI · UNIV OF ARKANSAS FOR MED SCIS · PI POST, STEVEN · 2004 to 2008
$1.4M
NHLBI NIH HHS R01HL075241NHLBI NIH HHS R01 HL089588NHLBI NIH HHS R01HL88588NIDDK NIH HHS DK07778
6 · The paper itself

Abstract

The importance of cytoplasmic motifs in differentially regulating SR-A function was demonstrated by deleting the first 49 cytoplasmic aa (SR-A(Delta1-49)), which abolished SR-A-mediated ligand internalization without reducing cell adhesion. To identify additional cytoplasmic motifs within the first 49 aa that regulate SR-A function, the acidic residues in a conserved motif (EDAD) were changed to their amide derivatives (SR-A(QNAN)). The function and regulation of SR-A(QNAN) were compared with that of SR-A(Delta1-49) and SR-A in transfected HEK-293 cells. Blocking PI3K activation inhibited SR-A, but not SR-A(Delta1-49)- or SR-A(QNAN)-mediated cell adhesion. Although deleting (SR-A(Delta1-49)) or mutating (SR-A(QNAN)) the EDAD motif abolished the PI3K sensitivity of SR-A-mediated cell adhesion, these mutations did not affect ligand internalization or PI3K activation during cell adhesion. To define the mechanism by which PI3K regulates SR-A-mediated cell adhesion, the cellular localization of wild-type and mutant SR-A was examined. PI3K inhibition reduced surface localization of SR-A but not of SR-A(Delta1-49) or SR-A(QNAN). The regulation of SR-A surface localization by PI3K was confirmed in peritoneal macrophages, which endogenously express SR-A. Together, these results suggest a pathway in which SR-A binding to an immobilized ligand activates PI3K to recruit more receptor to the plasma membrane and enhances cell adhesion.

Indexed as

Amino Acid MotifsAmino Acid SequenceAnimalsCell AdhesionCell LineCell MembraneCytoplasmEnzyme ActivationHumansLigandsMacrophages, PeritonealMiceMolecular Sequence DataPhosphatidylinositol 3-KinasesScavenger Receptors, Class AStructure-Activity RelationshipLigandsPhosphatidylinositol 3-KinasesScavenger Receptors, Class A

Identifiers

PMID19952357
PMCPMC2830124
OpenAlexW2097448205

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.