Evidence map›Paper›PMID 12417631›Full record

ArticleThe Journal of experimental medicine2002

Human autoimmune sera as molecular probes for the identification of an autoantigen kinase signaling pathway.

Makoto Kamachi, Truc M Le, Susan J Kim, Meghan E Geiger, Paul Anderson, Paul J Utz

Abstract read
In one paragraph

Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Article
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  16. Cell stress modulates the function of splicing regulatory protein RBM4 in translation control.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  17. Review
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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

6 authors.

Makoto KamachiDepartment of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Truc M Le
Susan J Kim
Meghan E Geiger
Paul Anderson
Paul J Utz

Funding

Strategies for Prevention of AutoimmunityU19DK061934 · NIDDK · STANFORD UNIVERSITY · PI FATHMAN, CHARLES GARRISON · 2001 to 2005
$4.4M
PHOSPHORYLATION OF LUPUS AUTOANTIGENS IN APOPTOSISK08AI001521 · NIAID · STANFORD UNIVERSITY · PI UTZ, PAUL JOSEPH · 1998 to 2002
$366k
NIAID NIH HHS K08AI01521NIDDK NIH HHS U19 DK061934NIDDK NIH HHS U19-DK61934
6 · The paper itself

Abstract

Using human autoimmune sera as molecular probes, we previously described the association of phosphorylated serine/arginine splicing factors (SR splicing factors) with the U1-small nuclear ribonucleoprotein (U1-snRNP) and U3-small nucleolar RNP (snoRNP) in apoptotic cells. SR proteins are highly conserved autoantigens whose activity is tightly regulated by reversible phosphorylation of serine residues by at least eight different SR protein kinase kinases (SRPKs), including SRPK1, SRPK2, and the scleroderma autoantigen topoisomerase I. In this report, we demonstrate that only one of the known SRPKs, SRPK1, is associated with the U1-snRNP autoantigen complex in healthy and apoptotic cells. SRPK1 is activated early during apoptosis, followed by caspase-mediated proteolytic inactivation at later time points. SRPKs are cleaved in vivo after multiple apoptotic stimuli, and cleavage can be inhibited by overexpression of bcl-2 and bcl-x(L), and by exposure to soluble peptide caspase inhibitors. Incubation of recombinant caspases with in vitro-translated SRPKs demonstrates that SRPK1 and SRPK2 are in vitro substrates for caspases-8 and -9, respectively. In contrast, topoisomerase I is cleaved by downstream caspases (-3 and -6). Since each of these SRPKs sits at a distinct checkpoint in the caspase cascade, SRPKs may serve an important role in signaling pathways governing apoptosis, alternative mRNA splicing, SR protein trafficking, RNA stability, and possibly the generation of autoantibodies directed against splicing factors.

Indexed as

ApoptosisAutoantibodiesAutoantigensbcl-X ProteinCaspasesDNA Topoisomerases, Type IEnzyme Activationfas ReceptorGene ExpressionHumansJurkat CellsLupus Erythematosus, SystemicMixed Connective Tissue DiseasePrecipitin TestsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-bcl-2AutoantibodiesAutoantigensBCL2L1 protein, humanbcl-X ProteinCaspasesDNA Topoisomerases, Type Ifas ReceptorProtein Serine-Threonine KinasesProto-Oncogene Proteins c-bcl-2Ribonucleoprotein, U1 Small NuclearSRPK1 protein, humanSRPK2 protein, human

Identifiers

PMID12417631
PMCPMC2194102

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Registered trials

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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.