Statements in which the resource exists.
SubjectPredicateObjectContext
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cpath:CPATH-64604http://www.biopax.org/relea...FUNCTION: Carries out a dual function: signal transduction and activation of transcription. Binds to the GAS element and activates PRL-induced transcription. SUBUNIT: Forms a homodimer or a heterodimer with a related family member. Binds NR3C1 (By similarity). Interacts with NCOA1, NMI and SOCS7. SUBCELLULAR LOCATION: Cytoplasm (By similarity). Nucleus (By similarity). Note=Translocated into the nucleus in response to phosphorylation (By similarity). PTM: Tyrosine phosphorylated in response to signaling via activated FLT3; wild-type FLT3 results in much weaker phosphorylation than constitutively activated mutant FLT3. Alternatively, can be phosporylated by JAK2. DISEASE: Defects in STAT5B are the cause of Laron type dwarfism II (LTD2) [MIM:245590]; also known as Laron syndrome type II or Laron syndrome due to a post-receptor defect. The phenotypic features are consistent with growth hormone deficiency in the presence of normal to elevated circulating concentrations of growth hormone, and resistance to hexogeneous hormone therapy. SIMILARITY: Belongs to the transcription factor STAT family. SIMILARITY: Contains 1 SH2 domain. WEB RESOURCE: Name=STAT5Bbase; Note=STAT5B mutation db; URL="http://bioinf.uta.fi/STAT5Bbase/"; WEB RESOURCE: Name=Wikipedia; Note=STAT5 entry; URL="http://en.wikipedia.org/wiki/STAT5"; COPYRIGHT: Protein annotation is derived from the UniProt Consortium (http://www.uniprot.org/). Distributed under the Creative Commons Attribution-NoDerivs License.lld:biogrid
cpath:CPATH-64604http://www.biopax.org/relea...FUNCTION: Carries out a dual function: signal transduction and activation of transcription. Binds to the GAS element and activates PRL-induced transcription. SUBUNIT: Forms a homodimer or a heterodimer with a related family member. Binds NR3C1 (By similarity). Interacts with NCOA1, NMI and SOCS7. SUBCELLULAR LOCATION: Cytoplasm (By similarity). Nucleus (By similarity). Note=Translocated into the nucleus in response to phosphorylation (By similarity). PTM: Tyrosine phosphorylated in response to signaling via activated FLT3; wild-type FLT3 results in much weaker phosphorylation than constitutively activated mutant FLT3. Alternatively, can be phosporylated by JAK2. DISEASE: Defects in STAT5B are the cause of Laron type dwarfism II (LTD2) [MIM:245590]; also known as Laron syndrome type II or Laron syndrome due to a post-receptor defect. The phenotypic features are consistent with growth hormone deficiency in the presence of normal to elevated circulating concentrations of growth hormone, and resistance to hexogeneous hormone therapy. SIMILARITY: Belongs to the transcription factor STAT family. SIMILARITY: Contains 1 SH2 domain. WEB RESOURCE: Name=STAT5Bbase; Note=STAT5B mutation db; URL="http://bioinf.uta.fi/STAT5Bbase/"; WEB RESOURCE: Name=Wikipedia; Note=STAT5 entry; URL="http://en.wikipedia.org/wiki/STAT5"; COPYRIGHT: Protein annotation is derived from the UniProt Consortium (http://www.uniprot.org/). Distributed under the Creative Commons Attribution-NoDerivs License.lld:cellmap
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