Evidence map›Paper›PMID 19827767›Full record

ArticleBiochemistry2009

Reengineering the signaling properties of a Src family kinase.

Shalini S Yadav, Brian J Yeh, Barbara P Craddock, Wendell A Lim, W Todd Miller

Open access · greenAbstract read
In one paragraph

Article in Biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Designing customized cell signalling circuits.Nature reviews. Molecular cell biology · 2010
    Review
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.

Shalini S YadavDepartment of Physiology and Biophysics, School of Medicine, Stony Brook University, Stony Brook, New York 11794-8661, USA.
Brian J Yeh
Barbara P Craddock
Wendell A Lim
W Todd Miller
Stony Brook University · USUniversity of California, San Francisco · US

Funding

SUSTRATE SPECIFICITY OF NONRECEPTOR TYROSINE KINASER01CA058530 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI MILLER, W TODD · 1999 to 2018
$3.7M
PROTEIN RECOGNITION IN SIGNAL TRANSDUCTIONR01GM055040 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LIM, WENDELL A · 1997 to 2015
$3.5M
SUBSTRATE SPECIFICITY OF NONRECEPTOR TYROSINE KINASESR29CA058530 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI MILLER, W TODD · 1993 to 1997
–
NCI NIH HHS CA58530NCI NIH HHS R01 CA058530NIGMS NIH HHS R01 GM055040
6 · The paper itself

Abstract

Src family kinases (SFKs) are modular signaling proteins possessing SH3, SH2, and tyrosine kinase domains. The SH3 and SH2 domains of SFKs have dual roles: they regulate the activity of the kinases, and they also target SFKs to their cellular substrates. We generated a series of novel SFKs by replacing the SH2 and SH3 domains of Hck with the syntrophin PDZ domain. In some constructs, the negative regulatory tyrosine in the C-terminal tail was also replaced with a PDZ ligand sequence. When expressed in mammalian cells, the substrate specificity of the PDZ-kinases was directed to a different group of proteins than wild-type Hck. The PDZ-kinases phosphorylate neuronal nitric oxide synthase (nNOS), a known binding partner of the syntrophin PDZ domain. We also introduced a PDZ ligand at the C-terminus of the adaptor protein Cas. PDZ-Hck kinases phosphorylate the engineered Cas protein in Cas(-/-) cells and restore the migration defect of these cells. A PDZ-kinase was also functional in rewiring MAPK signaling via an engineered ErbB2 construct containing a PDZ ligand sequence. Several of the PDZ-kinases show autoregulatory properties similar to natural SFKs. Thus, the PDZ-ligand interaction is able to functionally replace the normal SH2-pY527 interaction that regulates SFKs. Our data highlight the modularity and evolvability of signaling proteins.

Indexed as

Protein EngineeringSignal TransductionAnimalsCell Line, TransformedCell MovementChlorocebus aethiopsCOS CellsCrk-Associated Substrate ProteinDystrophin-Associated ProteinsErb-b2 Receptor Tyrosine KinasesMAP Kinase Signaling SystemMiceNitric Oxide Synthase Type IPDZ DomainsPhosphorylationProtein Interaction Domains and MotifsCrk-Associated Substrate ProteinDystrophin-Associated ProteinsErb-b2 Receptor Tyrosine KinasesNitric Oxide Synthase Type INos1 protein, mouseProto-Oncogene Proteins c-hckRecombinant Fusion Proteinssyntrophin

Identifiers

PMID19827767
PMCPMC2847435
OpenAlexW2162565357

What OpenQuestion holds

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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.