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SOCS3 is essential in the regulation of fetal liver erythropoiesis. Cell 1999 Sep 03;98(5):617-27

Date

09/18/1999

Pubmed ID

10490101

DOI

10.1016/s0092-8674(00)80049-5

Scopus ID

2-s2.0-0033520389   293 Citations

Abstract

SOCS3 (CIS3/JAB2) is an SH2-containing protein that binds to the activation loop of Janus kinases, inhibiting kinase activity, and thereby suppressing cytokine signaling. During embryonic development, SOCS3 is highly expressed in erythroid lineage cells and is Epo independent. Transgene-mediated expression blocks fetal erythropoiesis, resulting in embryonic lethality. SOCS3 deletion results in an embryonic lethality at 12-16 days associated with marked erythrocytosis. Moreover, the in vitro proliferative capacity of progenitors is greatly increased. SOCS3-deficient fetal liver stem cells can reconstitute hematopoiesis in lethally irradiated adults, indicating that its absence does not disturb bone marrow erythropoiesis. Reconstitution of lymphoid lineages in JAK3-deficient mice also occurs normally. The results demonstrate that SOCS3 is critical in negatively regulating fetal liver hematopoiesis.

Author List

Marine JC, McKay C, Wang D, Topham DJ, Parganas E, Nakajima H, Pendeville H, Yasukawa H, Sasaki A, Yoshimura A, Ihle JN

Author

Demin Wang PhD Assistant Professor in the Microbiology and Immunology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Dose-Response Relationship, Drug
Erythropoiesis
Flow Cytometry
Gene Expression Regulation, Developmental
Hematopoiesis
In Situ Hybridization
Interleukin-2
Interleukin-4
Liver
Mice
Mice, Mutant Strains
Models, Genetic
Mutagenesis
Phenotype
Proteins
Repressor Proteins
Suppressor of Cytokine Signaling 3 Protein
Suppressor of Cytokine Signaling Proteins
Time Factors
Transcription Factors
Transfection
jenkins-FCD Prod-398 336d56a365602aa89dcc112f077233607d6a5abc