| Predicate | Object |
|---|---|
| rdf:type | |
| http://www.biopax.org/relea... |
cpath:CPATH-LOCAL-265736,
cpath:CPATH-LOCAL-265736,
cpath:CPATH-LOCAL-265736,
cpath:CPATH-LOCAL-265737,
cpath:CPATH-LOCAL-265737,
cpath:CPATH-LOCAL-265737,
cpath:CPATH-LOCAL-265738,
cpath:CPATH-LOCAL-265738,
cpath:CPATH-LOCAL-265738,
cpath:CPATH-LOCAL-265739,
cpath:CPATH-LOCAL-265739,
cpath:CPATH-LOCAL-265739,
cpath:CPATH-LOCAL-265740,
cpath:CPATH-LOCAL-265740,
cpath:CPATH-LOCAL-265740,
cpath:CPATH-LOCAL-265741,
cpath:CPATH-LOCAL-265741,
cpath:CPATH-LOCAL-265741,
cpath:CPATH-LOCAL-265742,
cpath:CPATH-LOCAL-265742,
cpath:CPATH-LOCAL-265742,
cpath:CPATH-LOCAL-265743,
cpath:CPATH-LOCAL-265743,
cpath:CPATH-LOCAL-265743,
cpath:CPATH-LOCAL-265744,
cpath:CPATH-LOCAL-265744,
cpath:CPATH-LOCAL-265744,
cpath:CPATH-LOCAL-265745,
cpath:CPATH-LOCAL-265745,
cpath:CPATH-LOCAL-265745,
cpath:CPATH-LOCAL-265746,
cpath:CPATH-LOCAL-265746,
cpath:CPATH-LOCAL-265746,
cpath:CPATH-LOCAL-265747,
cpath:CPATH-LOCAL-265747,
cpath:CPATH-LOCAL-265747,
cpath:CPATH-LOCAL-265748,
cpath:CPATH-LOCAL-265748,
cpath:CPATH-LOCAL-265748,
cpath:CPATH-LOCAL-270554,
cpath:CPATH-LOCAL-270554,
cpath:CPATH-LOCAL-270554
|
| http://www.biopax.org/relea... |
Signal transducer and activator of transcription 1-alpha/beta,
Signal transducer and activator of transcription 1-alpha/beta,
Signal transducer and activator of transcription 1-alpha/beta
|
| http://www.biopax.org/relea... |
STAT1_HUMAN,
STAT1_HUMAN,
STAT1_HUMAN
|
| http://www.biopax.org/relea... | |
| http://www.biopax.org/relea... |
Transcription factor ISGF-3 components p91/p84,
Transcription factor ISGF-3 components p91/p84,
Transcription factor ISGF-3 components p91/p84
|
| http://www.biopax.org/relea... |
FUNCTION: Signal transducer and activator of transcription that mediates signaling by interferons (IFNs). Following type I IFN (IFN-alpha and IFN-beta) binding to cell surface receptors, Jak kinases (TYK2 and JAK1) are activated, leading to tyrosine phosphorylation of STAT1 and STAT2. The phosphorylated STATs dimerize, associate with ISGF3G/IRF-9 to form a complex termed ISGF3 transcription factor, that enters the nucleus. ISGF3 binds to the IFN stimulated response element (ISRE) to activate the transcription of interferon stimulated genes, which drive the cell in an antiviral state. In response to type II IFN (IFN-gamma), STAT1 is tyrosine- and serine-phosphorylated. It then forms a homodimer termed IFN-gamma-activated factor (GAF), migrates into the nucleus and binds to the IFN gamma activated sequence (GAS) to drive the expression of the target genes, inducing a cellular antiviral state. SUBUNIT: Isoform alpha homodimerizes upon IFN-gamma induced phosphorylation. Heterodimer with STAT2 upon IFN-alpha/beta induced phosphorylation. Interacts with NMI. Interacts with Sendai virus C', C, Y1 and Y2 proteins, Nipah virus P, V and W proteins, and rabies virus phosphoprotein preventing activation of ISRE and GAS promoter (By similarity). Interacts with HCV core protein; the interaction results in STAT1 degradation. Interacts with PIAS1; the interaction requires phosphorylation on Ser-727 and inhibits STAT1 activation. Interacts with IFNAR1; the interaction requires the phosphorylation of IFNAR1 at 'Tyr-466'. Interacts with IFNAR2. Interacts with PIAS1 (dimethylated on arginine); the interaction results in release of STAT1 from its target gene. SUBCELLULAR LOCATION: Cytoplasm. Nucleus. Note=Translocated into the nucleus in response to IFN-gamma-induced tyrosine phosphorylation and dimerization. ALTERNATIVE PRODUCTS: Event=Alternative splicing; Named isoforms=2; Name=Alpha; Synonyms=p91; IsoId=P42224-1; Sequence=Displayed; Name=Beta; Synonyms=p84; IsoId=P42224-2; Sequence=VSP_006282; PTM: Phosphorylated on tyrosine and serine residues in response to a variety of cytokines/growth hormones including IFN-alpha, IFN- gamma, PDGF and EGF. Upon EGF stimulation, phosphorylation on Tyr- 701 (lacking in beta form) by JAK1, JAK2 or TYK2 promotes dimerization and subsequent translocation to the nucleus. Growth hormone (GH) activates STAT1 signaling only via JAK2. PHosphorylation on Ser-727 by several kinases including MAPK14, ERK1/2 and CAMKII on IFN-gamma stimulation, regulates STAT1 transcriptional activity. Phosphorylation on Ser-727 promotes sumoylation though increasing interaction with PIAS. Phosphorylation on Ser-727 by PKCdelta induces apoptosis in response to DNA-damaging agents. PTM: Sumoylated by SUMO1, SUMO2 and SUMO3. Sumoylation is enhanced by IFN-gamma-induced phosphorylation on Ser-727, and by interaction with PIAS proteins. Enhances the transactivation activity. PTM: ISGylated. DISEASE: Note=STAT1 deficiency results in impaired immune response leading to severe mycobacterial and viral diseases. In the case of complete deficiency, patients can die of viral disease. DISEASE: Defects in STAT1 are a cause of mendelian susceptibility to mycobacterial disease (MSMD) [MIM:209950]; also known as familial disseminated atypical mycobacterial infection. This rare condition confers predisposition to illness caused by moderately virulent mycobacterial species, such as Bacillus Calmette-Guerin (BCG) vaccine and environmental non-tuberculous mycobacteria, and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections, with the exception of Salmonella which infects less than 50% of these individuals. The pathogenic mechanism underlying MSMD is the impairment of interferon-gamma mediated immunity whose severity determines the clinical outcome. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, whereas others develop, later in life, disseminated but curable infections with tuberculoid granulomas. MSMD is a genetically heterogeneous disease with autosomal recessive, autosomal dominant or X-linked inheritance. SIMILARITY: Belongs to the transcription factor STAT family. SIMILARITY: Contains 1 SH2 domain. WEB RESOURCE: Name=NIEHS-SNPs; URL="http://egp.gs.washington.edu/data/stat1/"; WEB RESOURCE: Name=STAT1base; Note=STAT1 mutation db; URL="http://bioinf.uta.fi/STAT1base/"; WEB RESOURCE: Name=Wikipedia; Note=STAT1 entry; URL="http://en.wikipedia.org/wiki/STAT1"; COPYRIGHT: Protein annotation is derived from the UniProt Consortium (http://www.uniprot.org/). Distributed under the Creative Commons Attribution-NoDerivs License.,
FUNCTION: Signal transducer and activator of transcription that mediates signaling by interferons (IFNs). Following type I IFN (IFN-alpha and IFN-beta) binding to cell surface receptors, Jak kinases (TYK2 and JAK1) are activated, leading to tyrosine phosphorylation of STAT1 and STAT2. The phosphorylated STATs dimerize, associate with ISGF3G/IRF-9 to form a complex termed ISGF3 transcription factor, that enters the nucleus. ISGF3 binds to the IFN stimulated response element (ISRE) to activate the transcription of interferon stimulated genes, which drive the cell in an antiviral state. In response to type II IFN (IFN-gamma), STAT1 is tyrosine- and serine-phosphorylated. It then forms a homodimer termed IFN-gamma-activated factor (GAF), migrates into the nucleus and binds to the IFN gamma activated sequence (GAS) to drive the expression of the target genes, inducing a cellular antiviral state. SUBUNIT: Isoform alpha homodimerizes upon IFN-gamma induced phosphorylation. Heterodimer with STAT2 upon IFN-alpha/beta induced phosphorylation. Interacts with NMI. Interacts with Sendai virus C', C, Y1 and Y2 proteins, Nipah virus P, V and W proteins, and rabies virus phosphoprotein preventing activation of ISRE and GAS promoter (By similarity). Interacts with HCV core protein; the interaction results in STAT1 degradation. Interacts with PIAS1; the interaction requires phosphorylation on Ser-727 and inhibits STAT1 activation. Interacts with IFNAR1; the interaction requires the phosphorylation of IFNAR1 at 'Tyr-466'. Interacts with IFNAR2. Interacts with PIAS1 (dimethylated on arginine); the interaction results in release of STAT1 from its target gene. SUBCELLULAR LOCATION: Cytoplasm. Nucleus. Note=Translocated into the nucleus in response to IFN-gamma-induced tyrosine phosphorylation and dimerization. ALTERNATIVE PRODUCTS: Event=Alternative splicing; Named isoforms=2; Name=Alpha; Synonyms=p91; IsoId=P42224-1; Sequence=Displayed; Name=Beta; Synonyms=p84; IsoId=P42224-2; Sequence=VSP_006282; PTM: Phosphorylated on tyrosine and serine residues in response to a variety of cytokines/growth hormones including IFN-alpha, IFN- gamma, PDGF and EGF. Upon EGF stimulation, phosphorylation on Tyr- 701 (lacking in beta form) by JAK1, JAK2 or TYK2 promotes dimerization and subsequent translocation to the nucleus. Growth hormone (GH) activates STAT1 signaling only via JAK2. PHosphorylation on Ser-727 by several kinases including MAPK14, ERK1/2 and CAMKII on IFN-gamma stimulation, regulates STAT1 transcriptional activity. Phosphorylation on Ser-727 promotes sumoylation though increasing interaction with PIAS. Phosphorylation on Ser-727 by PKCdelta induces apoptosis in response to DNA-damaging agents. PTM: Sumoylated by SUMO1, SUMO2 and SUMO3. Sumoylation is enhanced by IFN-gamma-induced phosphorylation on Ser-727, and by interaction with PIAS proteins. Enhances the transactivation activity. PTM: ISGylated. DISEASE: Note=STAT1 deficiency results in impaired immune response leading to severe mycobacterial and viral diseases. In the case of complete deficiency, patients can die of viral disease. DISEASE: Defects in STAT1 are a cause of mendelian susceptibility to mycobacterial disease (MSMD) [MIM:209950]; also known as familial disseminated atypical mycobacterial infection. This rare condition confers predisposition to illness caused by moderately virulent mycobacterial species, such as Bacillus Calmette-Guerin (BCG) vaccine and environmental non-tuberculous mycobacteria, and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections, with the exception of Salmonella which infects less than 50% of these individuals. The pathogenic mechanism underlying MSMD is the impairment of interferon-gamma mediated immunity whose severity determines the clinical outcome. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, whereas others develop, later in life, disseminated but curable infections with tuberculoid granulomas. MSMD is a genetically heterogeneous disease with autosomal recessive, autosomal dominant or X-linked inheritance. SIMILARITY: Belongs to the transcription factor STAT family. SIMILARITY: Contains 1 SH2 domain. WEB RESOURCE: Name=NIEHS-SNPs; URL="http://egp.gs.washington.edu/data/stat1/"; WEB RESOURCE: Name=STAT1base; Note=STAT1 mutation db; URL="http://bioinf.uta.fi/STAT1base/"; WEB RESOURCE: Name=Wikipedia; Note=STAT1 entry; URL="http://en.wikipedia.org/wiki/STAT1"; COPYRIGHT: Protein annotation is derived from the UniProt Consortium (http://www.uniprot.org/). Distributed under the Creative Commons Attribution-NoDerivs License.,
FUNCTION: Signal transducer and activator of transcription that mediates signaling by interferons (IFNs). Following type I IFN (IFN-alpha and IFN-beta) binding to cell surface receptors, Jak kinases (TYK2 and JAK1) are activated, leading to tyrosine phosphorylation of STAT1 and STAT2. The phosphorylated STATs dimerize, associate with ISGF3G/IRF-9 to form a complex termed ISGF3 transcription factor, that enters the nucleus. ISGF3 binds to the IFN stimulated response element (ISRE) to activate the transcription of interferon stimulated genes, which drive the cell in an antiviral state. In response to type II IFN (IFN-gamma), STAT1 is tyrosine- and serine-phosphorylated. It then forms a homodimer termed IFN-gamma-activated factor (GAF), migrates into the nucleus and binds to the IFN gamma activated sequence (GAS) to drive the expression of the target genes, inducing a cellular antiviral state. SUBUNIT: Isoform alpha homodimerizes upon IFN-gamma induced phosphorylation. Heterodimer with STAT2 upon IFN-alpha/beta induced phosphorylation. Interacts with NMI. Interacts with Sendai virus C', C, Y1 and Y2 proteins, Nipah virus P, V and W proteins, and rabies virus phosphoprotein preventing activation of ISRE and GAS promoter (By similarity). Interacts with HCV core protein; the interaction results in STAT1 degradation. Interacts with PIAS1; the interaction requires phosphorylation on Ser-727 and inhibits STAT1 activation. Interacts with IFNAR1; the interaction requires the phosphorylation of IFNAR1 at 'Tyr-466'. Interacts with IFNAR2. Interacts with PIAS1 (dimethylated on arginine); the interaction results in release of STAT1 from its target gene. SUBCELLULAR LOCATION: Cytoplasm. Nucleus. Note=Translocated into the nucleus in response to IFN-gamma-induced tyrosine phosphorylation and dimerization. ALTERNATIVE PRODUCTS: Event=Alternative splicing; Named isoforms=2; Name=Alpha; Synonyms=p91; IsoId=P42224-1; Sequence=Displayed; Name=Beta; Synonyms=p84; IsoId=P42224-2; Sequence=VSP_006282; PTM: Phosphorylated on tyrosine and serine residues in response to a variety of cytokines/growth hormones including IFN-alpha, IFN- gamma, PDGF and EGF. Upon EGF stimulation, phosphorylation on Tyr- 701 (lacking in beta form) by JAK1, JAK2 or TYK2 promotes dimerization and subsequent translocation to the nucleus. Growth hormone (GH) activates STAT1 signaling only via JAK2. PHosphorylation on Ser-727 by several kinases including MAPK14, ERK1/2 and CAMKII on IFN-gamma stimulation, regulates STAT1 transcriptional activity. Phosphorylation on Ser-727 promotes sumoylation though increasing interaction with PIAS. Phosphorylation on Ser-727 by PKCdelta induces apoptosis in response to DNA-damaging agents. PTM: Sumoylated by SUMO1, SUMO2 and SUMO3. Sumoylation is enhanced by IFN-gamma-induced phosphorylation on Ser-727, and by interaction with PIAS proteins. Enhances the transactivation activity. PTM: ISGylated. DISEASE: Note=STAT1 deficiency results in impaired immune response leading to severe mycobacterial and viral diseases. In the case of complete deficiency, patients can die of viral disease. DISEASE: Defects in STAT1 are a cause of mendelian susceptibility to mycobacterial disease (MSMD) [MIM:209950]; also known as familial disseminated atypical mycobacterial infection. This rare condition confers predisposition to illness caused by moderately virulent mycobacterial species, such as Bacillus Calmette-Guerin (BCG) vaccine and environmental non-tuberculous mycobacteria, and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections, with the exception of Salmonella which infects less than 50% of these individuals. The pathogenic mechanism underlying MSMD is the impairment of interferon-gamma mediated immunity whose severity determines the clinical outcome. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, whereas others develop, later in life, disseminated but curable infections with tuberculoid granulomas. MSMD is a genetically heterogeneous disease with autosomal recessive, autosomal dominant or X-linked inheritance. SIMILARITY: Belongs to the transcription factor STAT family. SIMILARITY: Contains 1 SH2 domain. WEB RESOURCE: Name=NIEHS-SNPs; URL="http://egp.gs.washington.edu/data/stat1/"; WEB RESOURCE: Name=STAT1base; Note=STAT1 mutation db; URL="http://bioinf.uta.fi/STAT1base/"; WEB RESOURCE: Name=Wikipedia; Note=STAT1 entry; URL="http://en.wikipedia.org/wiki/STAT1"; COPYRIGHT: Protein annotation is derived from the UniProt Consortium (http://www.uniprot.org/). Distributed under the Creative Commons Attribution-NoDerivs License.
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| skos:exactMatch | |
| skos:closeMatch |