Evidence map›Paper›PMID 26026062›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

The Tec Kinase-Regulated Phosphoproteome Reveals a Mechanism for the Regulation of Inhibitory Signals in Murine Macrophages.

Giacomo Tampella, Hannah M Kerns, Deqiang Niu, Swati Singh, Socheath Khim, Katherine A Bosch, Meghan E Garrett, Albanus Moguche, Erica Evans, Beth Browning and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. 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
1.3field-weighted citation impact, top 22% 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, 19 citations in OpenAlex.

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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

17 authors at 5 institutions in 3 countries.

Giacomo TampellaSeattle Children's Research Institute, Seattle WA 98101;
Hannah M KernsSeattle Children's Research Institute, Seattle WA 98101;
Deqiang NiuCelgene Avilomics Research, Bedford, MA 01730;
Swati SinghSeattle Children's Research Institute, Seattle WA 98101;
Socheath KhimSeattle Children's Research Institute, Seattle WA 98101;
Katherine A BoschSeattle Children's Research Institute, Seattle WA 98101;
Meghan E GarrettSeattle Children's Research Institute, Seattle WA 98101;
Albanus MogucheSeattle Children's Research Institute, Seattle WA 98101; Department of Immunology, University of Washington School of Medicine, Seattle WA 98195;
Erica EvansCelgene Avilomics Research, Bedford, MA 01730;
Beth BrowningCelgene Avilomics Research, Bedford, MA 01730;
Tahmina A JahanDepartment of Genome Sciences, University of Washington School of Medicine, Seattle WA 98195;
Mariana NachtCelgene Avilomics Research, Bedford, MA 01730;
Alejandro Wolf-YadlinDepartment of Genome Sciences, University of Washington School of Medicine, Seattle WA 98195;
Alessandro PlebaniExperimental Sciences, Pediatrics Clinic and Institute for Molecular Medicine A. Nocivelli, University of Brescia, Civil Hospital of Brescia, 25100 Bescia, Italy;
Jessica A HamermanDepartment of Immunology, University of Washington School of Medicine, Seattle WA 98195; Benaroya Research Institute, Seattle WA 98101; and.
David J RawlingsSeattle Children's Research Institute, Seattle WA 98101; Department of Immunology, University of Washington School of Medicine, Seattle WA 98195; Department of Pediatrics, University of Washington School of Medicine, Seattle WA 98195 drawling@uw.edu rickerj@uw.edu.
Richard G JamesSeattle Children's Research Institute, Seattle WA 98101; Department of Pediatrics, University of Washington School of Medicine, Seattle WA 98195 drawling@uw.edu rickerj@uw.edu.
University of Washington · USBristol-Myers Squibb (Switzerland) · CHSeattle Children's Hospital · USCenter for Infectious Disease Research · USBrescia University · US

Funding

Lentiviral Gene Therapy for Wiskott-Aldrich SyndromeR01AI071163 · NIAID · SEATTLE CHILDREN'S HOSPITAL · PI RAWLINGS, DAVID J · 2008 to 2012
$3.5M
REGULATION OF B CELL DEVELOPMENT AND SIGNALING BY BTKR01HD037091 · NICHD · UNIVERSITY OF WASHINGTON · PI RAWLINGS, DAVID J · 1999 to 2008
$2.7M
Lentiviral Gene Therapy of X-Linked AgammaglobulinemiaR01AI084457 · NIAID · SEATTLE CHILDREN'S HOSPITAL · PI RAWLINGS, DAVID J · 2012 to 2015
$2.5M
Regulation of Inflammatory Signaling during the Innate Immune ResponseR01AI073441 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI HAMERMAN, JESSICA A · 2007 to 2011
$2.4M
Lentiviral Gene Therapy of X-linked AgammaglobulinemiaR01HL075453 · NHLBI · SEATTLE CHILDREN'S HOSPITAL · PI RAWLINGS, DAVID J · 2004 to 2008
$1.9M
In vivo role of BTK-mediated inhibition of Wnt/b-catenin signaling during hematopR00HL103768 · NHLBI · SEATTLE CHILDREN'S HOSPITAL · PI JAMES, RICHARD GOFF · 2012 to 2014
$717k
In vivo role of BTK-mediated inhibition of Wnt/b-catenin signaling during hematopK99HL103768 · NHLBI · UNIVERSITY OF WASHINGTON · PI JAMES, RICHARD GOFF · 2010 to 2011
$254k
NHLBI NIH HHS K99 HL103768NHLBI NIH HHS R00 HL103768NHLBI NIH HHS R00HL103768NHLBI NIH HHS R01HL075453NIAID NIH HHS R01AI071163NIAID NIH HHS R01 AI073441NIAID NIH HHS R01AI073441NIAID NIH HHS R01 AI084457NIAID NIH HHS R01AI084457NICHD NIH HHS R01HD037091
6 · The paper itself

Abstract

Previous work has shown conflicting roles for Tec family kinases in regulation of TLR-dependent signaling in myeloid cells. In the present study, we performed a detailed investigation of the role of the Tec kinases Btk and Tec kinases in regulating TLR signaling in several types of primary murine macrophages. We demonstrate that primary resident peritoneal macrophages deficient for Btk and Tec secrete less proinflammatory cytokines in response to TLR stimulation than do wild-type cells. In contrast, we found that bone marrow-derived and thioglycollate-elicited peritoneal macrophages deficient for Btk and Tec secrete more proinflammatory cytokines than do wild-type cells. We then compared the phosphoproteome regulated by Tec kinases and LPS in primary peritoneal and bone marrow-derived macrophages. From this analysis we determined that Tec kinases regulate different signaling programs in these cell types. In additional studies using bone marrow-derived macrophages, we found that Tec and Btk promote phosphorylation events necessary for immunoreceptor-mediated inhibition of TLR signaling. Taken together, our results are consistent with a model where Tec kinases (Btk, Tec, Bmx) are required for TLR-dependent signaling in many types of myeloid cells. However, our data also support a cell type-specific TLR inhibitory role for Btk and Tec that is mediated by immunoreceptor activation and signaling via PI3K.

Indexed as

Agammaglobulinaemia Tyrosine KinaseAnimalsBone Marrow CellsGene Expression ProfilingGene Expression RegulationLipopolysaccharidesMacrophagesMiceMice, Inbred C57BLMice, KnockoutOrgan SpecificityPeritoneal CavityPhosphatidylinositol 3-KinasesPhosphoproteinsPhosphorylationPrimary Cell CultureAgammaglobulinaemia Tyrosine KinaseBmx protein, mouseLipopolysaccharidesPhosphatidylinositol 3-KinasesPhosphoproteinsProtein-Tyrosine KinasesTec protein-tyrosine kinaseToll-Like Receptors

Identifiers

PMID26026062
PMCPMC4475445
OpenAlexW1573843383

What OpenQuestion holds

Textmetadata
LicenceTDM
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.