SOCS3 is essential in the regulation of fetal liver erythropoiesis (Q28144536)

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C McKay

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D Wang

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D J Topham

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E Parganas

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H Nakajima

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H Pendeville

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H Yasukawa

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A Sasaki

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A Yoshimura

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J N Ihle

Growth hormone preferentially induces the rapid, transient expression of SOCS-3, a novel inhibitor of cytokine receptor signaling

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language of work or name

English

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publication date

3 September 1999

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published in

Cell

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volume

98

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issue

5

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page(s)

617-27

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cites work

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Interleukin-11 stimulates proopiomelanocortin gene expression and adrenocorticotropin secretion in corticotroph cells: evidence for a redundant cytokine network in the hypothalamo-pituitary-adrenal axis

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Autoregulation of pituitary corticotroph SOCS-3 expression: characterization of the murine SOCS-3 promoter

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DNA ligase I is required for fetal liver erythropoiesis but is not essential for mammalian cell viability

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Identification of SOCS-3 as a potential mediator of central leptin resistance

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SOCS-3 is tyrosine phosphorylated in response to interleukin-2 and suppresses STAT5 phosphorylation and lymphocyte proliferation

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Differential requirement for caspase 9 in apoptotic pathways in vivo.

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A developmental switch in thymic lymphocyte maturation potential occurs at the level of hematopoietic stem cells

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The Elongin BC complex interacts with the conserved SOCS-box motif present in members of the SOCS, ras, WD-40 repeat, and ankyrin repeat families

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Specific recruitment of SH-PTP1 to the erythropoietin receptor causes inactivation of JAK2 and termination of proliferative signals

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Bcl-2 rescues T lymphopoiesis, but not B or NK cell development, in common gamma chain-deficient mice

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SOCS1 deficiency causes a lymphocyte-dependent perinatal lethality

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Massive cell death of immature hematopoietic cells and neurons in Bcl-x-deficient mice

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Accelerated apoptosis of lymphocytes by augmented induction of Bax in SSI-1 (STAT-induced STAT inhibitor-1) deficient mice

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Jak2 deficiency defines an essential developmental checkpoint in definitive hematopoiesis

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Genetics of erythropoiesis: induced mutations in mice and zebrafish

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Jak2 is essential for signaling through a variety of cytokine receptors

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Fetal anemia and apoptosis of red cell progenitors in Stat5a-/-5b-/- mice: a direct role for Stat5 in Bcl-X(L) induction

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The suppressor of cytokine signaling (SOCS) 1 and SOCS3 but not SOCS2 proteins inhibit interferon-mediated antiviral and antiproliferative activities

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A family of cytokine-inducible inhibitors of signalling

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Liver degeneration and lymphoid deficiencies in mice lacking suppressor of cytokine signaling-1.

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Stat5a and Stat5b proteins have essential and nonessential, or redundant, roles in cytokine responses

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Modulation of gene activity by consecutive gene targeting of one creatine kinase M allele in mouse embryonic stem cells

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Skeletal muscles of mice deficient in muscle creatine kinase lack burst activity

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Targeted disruption of the mouse Caspase 8 gene ablates cell death induction by the TNF receptors, Fas/Apo1, and DR3 and is lethal prenatally.

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Interaction of the erythropoietin and stem-cell-factor receptors

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Generation of committed erythroid BFU-E and CFU-E progenitors does not require erythropoietin or the erythropoietin receptor

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The JAK-binding protein JAB inhibits Janus tyrosine kinase activity through binding in the activation loop

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FADD: essential for embryo development and signaling from some, but not all, inducers of apoptosis

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The conserved SOCS box motif in suppressors of cytokine signaling binds to elongins B and C and may couple bound proteins to proteasomal degradation

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