Evidence map›Paper›PMID 15988034›Full record

ArticleMolecular and cellular biology2005

Inhibiting myosin light chain kinase induces apoptosis in vitro and in vivo.

Fabeha Fazal, Lianzhi Gu, Ivanna Ihnatovych, Yoojeong Han, WenYang Hu, Nenad Antic, Fernando Carreira, James F Blomquist, Thomas J Hope, David S Ucker and 1 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

42 citing papers in PubMed, 77 citations in OpenAlex.

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  19. Temporal Heterogeneity Metrics in Apoptosis Induced by Anticancer Drugs.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2015
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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

11 authors at 1 institution in 1 country.

Fabeha FazalDepartment of Physiology and Biophysics, College of Medicine, University of Illinois at Chicago, 835 South Wolcott Avenue, Chicago, Illinois 60612, USA.
Lianzhi Gu
Ivanna Ihnatovych
Yoojeong Han
WenYang Hu
Nenad Antic
Fernando Carreira
James F Blomquist
Thomas J Hope
David S Ucker
Primal de Lanerolle
University of Illinois Chicago · US

Funding

INTRACELLULAR TRAFFICKING OF HIV-1 PARTICLESR01AI047770 · NIAID · UNIVERSITY OF ILLINOIS AT CHICAGO · PI HOPE, THOMAS · 2000 to 2010
$2.9M
GTPase Regulation of Smooth Muscle ContractionR01HL064702 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DE LANEROLLE, PRIMAL · 2001 to 2004
$1.4M
MYOSIN LIGHT CHAIN KINASE IN SMOOTH MUSCLE PROLIFERATIONR01HL059618 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DE LANEROLLE, PRIMAL · 1998 to 2002
$837k
ACTIVATION OF TARGET CELL SUICIDE IN THE IMMUNE SYSTEMR01GM038800 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI UCKER, DAVID S · 1988 to 2002
$790k
Intracellular Trafficking of HIV-1 ParticlesR56AI047770 · NIAID · NORTHWESTERN UNIVERSITY · PI HOPE, THOMAS · 2005 to 2005
$336k
MLC Dephosphorylation in Smooth Muscle Cell ApoptosisF32HL068458 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FAZAL, FABEHA · 2002 to 2002
$54k
NHLBI NIH HHS F32 HL068458NHLBI NIH HHS HL 59618NHLBI NIH HHS HL 64702NHLBI NIH HHS HL68458NHLBI NIH HHS R01 HL059618NHLBI NIH HHS R01 HL064702NIAID NIH HHS AI47770NIAID NIH HHS R01 AI047770NIAID NIH HHS R56 AI047770NIGMS NIH HHS GM 38800
6 · The paper itself

Abstract

Previous short-term studies have correlated an increase in the phosphorylation of the 20-kDa light chain of myosin II (MLC20) with blebbing in apoptotic cells. We have found that this increase in MLC20 phosphorylation is rapidly followed by MLC20 dephosphorylation when cells are stimulated with various apoptotic agents. MLC20 dephosphorylation is not a consequence of apoptosis because MLC20 dephosphorylation precedes caspase activation when cells are stimulated with a proapoptotic agent or when myosin light chain kinase (MLCK) is inhibited pharmacologically or by microinjecting an inhibitory antibody to MLCK. Moreover, blocking caspase activation increased cell survival when MLCK is inhibited or when cells are treated with tumor necrosis factor alpha. Depolymerizing actin filaments or detaching cells, processes that destabilize the cytoskeleton, or inhibiting myosin ATPase activity also resulted in MLC20 dephosphorylation and cell death. In vivo experiments showed that inhibiting MLCK increased the number of apoptotic cells and retarded the growth of mammary cancer cells in mice. Thus, MLC20 dephosphorylation occurs during physiological cell death and prolonged MLC20 dephosphorylation can trigger apoptosis.

Indexed as

ApoptosisAnimalsAntibodiesCaspase 3Caspase InhibitorsCaspasesCells, CulturedCytoskeletonHumansMiceMyosin-Light-Chain KinaseMyosin Light ChainsMyosin Type IIPhosphorylationAntibodiesCASP3 protein, humanCasp3 protein, mouseCaspase 3Caspase InhibitorsCaspasesMyosin-Light-Chain KinaseMyosin Light ChainsMyosin Type II

Identifiers

PMID15988034
PMCPMC1168802
OpenAlexW2070335110

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.