Evidence map›Paper›PMID 30917487›Full record

ReviewInternational journal of molecular sciences2019

The Role of Tyrosine Phosphorylation of Protein Kinase C Delta in Infection and Inflammation.

Qingliang Yang, Jordan C Langston, Yuan Tang, Mohammad F Kiani, Laurie E Kilpatrick

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  9. Anti-Neuroinflammatory Effects ofInternational journal of molecular sciences · 2024
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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

5 authors at 1 institution in 1 country.

Qingliang YangDepartment of Mechanical Engineering, College of Engineering, Temple University, Philadelphia, PA 19122, USA. tug44932@temple.edu.
Jordan C LangstonDepartment of Bioengineering, College of Engineering, Temple University, Philadelphia, PA 19122, USA. tuj27061@temple.edu.
Yuan TangDepartment of Mechanical Engineering, College of Engineering, Temple University, Philadelphia, PA 19122, USA. tud19329@temple.edu.
Mohammad F KianiDepartment of Mechanical Engineering, College of Engineering, Temple University, Philadelphia, PA 19122, USA. mkiani@temple.edu.
Laurie E KilpatrickCenter for Inflammation, Clinical and Translational Lung Research, Department of Thoracic Medicine and Surgery, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA. laurie.kilpatrick@temple.edu.ORCID 0000-0002-2554-507X
Temple University · US

Funding

Leukocyte-Endothelial Cell Interactions in SepsisR01GM114359 · NIGMS · TEMPLE UNIV OF THE COMMONWEALTH · PI KIANI, MOHAMMAD F, KILPATRICK, LAURIE E · 2015 to 2018
$1.2M
Integrating microfluidic, omic, and in silico models to screen therapeutics for sepsisR01GM134701 · NIGMS · TEMPLE UNIV OF THE COMMONWEALTH · PI KIANI, MOHAMMAD F, KILPATRICK, LAURIE E · 2019 to 2020
$656k
American Heart Association 16GRNT29980001National Institute of Health GM114359NIGMS NIH HHS R01 GM114359NIGMS NIH HHS R01 GM134701
6 · The paper itself

Abstract

Protein Kinase C (PKC) is a family composed of phospholipid-dependent serine/threonine kinases that are master regulators of inflammatory signaling. The activity of different PKCs is context-sensitive and these kinases can be positive or negative regulators of signaling pathways. The delta isoform (PKCδ) is a critical regulator of the inflammatory response in cancer, diabetes, ischemic heart disease, and neurodegenerative diseases. Recent studies implicate PKCδ as an important regulator of the inflammatory response in sepsis. PKCδ, unlike other members of the PKC family, is unique in its regulation by tyrosine phosphorylation, activation mechanisms, and multiple subcellular targets. Inhibition of PKCδ may offer a unique therapeutic approach in sepsis by targeting neutrophil-endothelial cell interactions. In this review, we will describe the overall structure and function of PKCs, with a focus on the specific phosphorylation sites of PKCδ that determine its critical role in cell signaling in inflammatory diseases such as sepsis. Current genetic and pharmacological tools, as well as in vivo models, that are used to examine the role of PKCδ in inflammation and sepsis are presented and the current state of emerging tools such as microfluidic assays in these studies is described.

Indexed as

Signal TransductionAllosteric RegulationAnimalsHumansNeutrophilsPhosphorylationProtein Kinase C-deltaSepsisProtein Kinase C-deltainflammationmicrofluidicsphosphorylationPKCPKCδsepsis

Identifiers

PMID30917487
PMCPMC6471617
OpenAlexW2923005193

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.