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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004485naa a2201009 4500
001oai:gup.ub.gu.se/75210
003SwePub
008240528s2005 | |||||||||||000 ||eng|
024a https://gup.ub.gu.se/publication/752102 URI
024a https://doi.org/10.1172/JCI227102 DOI
024a https://doi.org/10.1172/JCI2005227102 DOI
040 a (SwePub)gu
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Greenhalgh, Christopher J4 aut
2451 0a SOCS2 negatively regulates growth hormone action in vitro and in vivo.
264 1c 2005
520 a Mice deficient in SOCS2 display an excessive growth phenotype characterized by a 30-50% increase in mature body size. Here we show that the SOCS2-/- phenotype is dependent upon the presence of endogenous growth hormone (GH) and that treatment with exogenous GH induced excessive growth in mice lacking both endogenous GH and SOCS2. This was reflected in terms of overall body weight, body and bone lengths, and the weight of internal organs and tissues. A heightened response to GH was also measured by examining GH-responsive genes expressed in the liver after exogenous GH administration. To further understand the link between SOCS2 and the GH-signaling cascade, we investigated the nature of these interactions using structure/function and biochemical interaction studies. Analysis of the 3 structural motifs of the SOCS2 molecule revealed that each plays a crucial role in SOCS2 function, with the conserved SOCS-box motif being essential for all inhibitory function. SOCS2 was found to bind 2 phosphorylated tyrosines on the GH receptor, and mutational analysis of these amino acids showed that both were essential for SOCS2 function. Together, the data provide clear evidence that SOCS2 is a negative regulator of GH signaling.
653 a Amino Acid Motifs
653 a genetics
653 a Animals
653 a Body Weight
653 a drug effects
653 a genetics
653 a physiology
653 a DNA-Binding Proteins
653 a genetics
653 a metabolism
653 a Gene Expression Regulation
653 a genetics
653 a physiology
653 a Growth Hormone
653 a administration & dosage
653 a genetics
653 a physiology
653 a Insulin-Like Growth Factor I
653 a physiology
653 a Liver
653 a metabolism
653 a pathology
653 a Mice
653 a Mice
653 a Knockout
653 a Phosphorylation
653 a Protein Binding
653 a genetics
653 a physiology
653 a Receptors
653 a Somatotropin
653 a genetics
653 a metabolism
653 a Repressor Proteins
653 a genetics
653 a metabolism
653 a Signal Transduction
653 a drug effects
653 a genetics
653 a physiology
653 a Suppressor of Cytokine Signaling Proteins
653 a Trans-Activators
653 a genetics
653 a metabolism
653 a Tyrosine
653 a metabolism
700a Rico-Bautista, Elizabeth4 aut
700a Lorentzon, Mattias,d 1970u Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin,Institute of Internal Medicine4 aut0 (Swepub:gu)xlomat
700a Thaus, Anne L4 aut
700a Morgan, Phillip O4 aut
700a Willson, Tracy A4 aut
700a Zervoudakis, Panagiota4 aut
700a Metcalf, Donald4 aut
700a Street, Ian4 aut
700a Nicola, Nicos A4 aut
700a Nash, Andrew D4 aut
700a Fabri, Louis J4 aut
700a Norstedt, Gunnar4 aut
700a Ohlsson, Claes,d 1965u Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för internmedicin,Institute of Internal Medicine, Dept of Medicine4 aut0 (Swepub:gu)xohlcl
700a Flores-Morales, Amilcar4 aut
700a Alexander, Warren S4 aut
700a Hilton, Douglas J4 aut
710a Göteborgs universitetb Institutionen för invärtesmedicin4 org
773t The Journal of clinical investigationg 115:2, s. 397-406q 115:2<397-406x 0021-9738
8564 8u https://gup.ub.gu.se/publication/75210
8564 8u https://doi.org/10.1172/JCI22710
8564 8u https://doi.org/10.1172/JCI200522710

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