Evidence map›Paper›PMID 28546428›Full record

ArticleThe Journal of biological chemistry2017

The myocardin-related transcription factor MKL co-regulates the cellular levels of two profilin isoforms.

Marion Joy, David Gau, Nevin Castellucci, Ron Prywes, Partha Roy

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. 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

5 authors at 2 institutions in 1 country.

Marion JoyDepartments of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania 15219.
David GauDepartments of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania 15219.
Nevin CastellucciDepartments of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania 15219.
Ron PrywesDepartment of Biological Sciences, Columbia University, New York, New York 10027.
Partha RoyDepartments of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania 15219; Cell Biology, University of Pittsburgh, Pittsburgh, Pennsylvania 15219; Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania 15219. Electronic address: par19@pitt.edu.
University of Pittsburgh · USColumbia University · US

Funding

Cardiovascular Bioengineering Training ProgramT32HL076124 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SANJEEV G SHROFF · 2005 to 2026
$7.0M
Profilin as a target to suppress Invasive breast cancerR01CA108607 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ROY, PARTHA · 2006 to 2017
$2.6M
NCI NIH HHS R01 CA108607NHLBI NIH HHS T32 HL076124
6 · The paper itself

Abstract

Megakaryoblastic leukemia (MKL)/serum-response factor (SRF)-mediated gene transcription is a highly conserved mechanism that connects dynamic reorganization of the actin cytoskeleton to regulation of expression of a wide range of genes, including SRF itself and many important structural and regulatory components of the actin cytoskeleton. In this study, we examined the possible role of MKL/SRF in the context of regulation of profilin (Pfn), a major controller of actin dynamics and actin cytoskeletal remodeling in cells. We demonstrated that despite being located on different genomic loci, two major isoforms of Pfn (Pfn1 and Pfn2) are co-regulated by a common mechanism involving the action of MKL that is independent of its SRF-related activity. We found that MKL co-regulates the expression of Pfn isoforms indirectly by modulating signal transducer and activator of transcription 1 (STAT1) and utilizing its SAP-domain function. Unexpectedly, our studies revealed that cellular externalization, rather than transcription of Pfn1, is affected by the perturbations of MKL. We further demonstrated that MKL can influence cell migration by modulating Pfn1 expression, indicating a functional connection between MKL and Pfn1 in actin-dependent cellular processes. Finally, we provide initial evidence supporting the ability of Pfn to influence MKL and SRF expression. Collectively, these findings suggest that Pfn may play a role in a possible feedback loop of the actin/MKL/SRF signaling circuit.

Indexed as

Gene Expression RegulationCell Line, TumorCell MovementHEK293 CellsHumansOligopeptidesProfilinsProtein Interaction Domains and MotifsProtein TransportRecombinant Fusion ProteinsRNA InterferenceRNA, MessengerSerum Response FactorSTAT1 Transcription FactorTrans-ActivatorsFLAG peptideMRTFA protein, humanOligopeptidesPFN1 protein, humanPFN2 protein, humanProfilinsRecombinant Fusion ProteinsRNA, MessengerSerum Response FactorSRF protein, humanSTAT1 protein, humanSTAT1 Transcription FactorTrans-Activatorsactincell migrationcytoskeletonMKLprofilinSAP-domainserum-response factor (SRF)

Identifiers

PMID28546428
PMCPMC5512072
OpenAlexW2619643387

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.