4k81: Difference between revisions

Line 1:

~~'''Unreleased~~ structure~~'''~~

===Crystal structure of the Grb14 RA and PH domains in complex with GTP-loaded H-Ras===

~~The~~ entry ~~4k81~~ is ~~ON HOLD~~ ~~until Paper Publication~~

==Disease==

[[http://www.uniprot.org/uniprot/RASH_HUMAN RASH_HUMAN]] Defects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS) [MIM:[http://omim.org/entry/218040 218040]]. A rare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities (typically pulmonic stenosis, hypertrophic cardiomyopathy and/or atrial tachycardia), tumor predisposition, skin and musculoskeletal abnormalities.<ref>PMID:16170316</ref> <ref>PMID:16329078</ref> <ref>PMID:16443854</ref> <ref>PMID:17054105</ref> <ref>PMID:18247425</ref> <ref>PMID:18039947</ref> <ref>PMID:19995790</ref> Defects in HRAS are the cause of congenital myopathy with excess of muscle spindles (CMEMS) [MIM:[http://omim.org/entry/218040 218040]]. CMEMS is a variant of Costello syndrome.<ref>PMID:17412879</ref> Defects in HRAS may be a cause of susceptibility to Hurthle cell thyroid carcinoma (HCTC) [MIM:[http://omim.org/entry/607464 607464]]. Hurthle cell thyroid carcinoma accounts for approximately 3% of all thyroid cancers. Although they are classified as variants of follicular neoplasms, they are more often multifocal and somewhat more aggressive and are less likely to take up iodine than are other follicular neoplasms. Note=Mutations which change positions 12, 13 or 61 activate the potential of HRAS to transform cultured cells and are implicated in a variety of human tumors. Defects in HRAS are a cause of susceptibility to bladder cancer (BLC) [MIM:[http://omim.org/entry/109800 109800]]. A malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and at different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin, flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences. Note=Defects in HRAS are the cause of oral squamous cell carcinoma (OSCC).<ref>PMID:1459726</ref> Defects in HRAS are the cause of Schimmelpenning-Feuerstein-Mims syndrome (SFM) [MIM:[http://omim.org/entry/163200 163200]]. A disease characterized by sebaceous nevi, often on the face, associated with variable ipsilateral abnormalities of the central nervous system, ocular anomalies, and skeletal defects. Many oral manifestations have been reported, not only including hypoplastic and malformed teeth, and mucosal papillomatosis, but also ankyloglossia, hemihyperplastic tongue, intraoral nevus, giant cell granuloma, ameloblastoma, bone cysts, follicular cysts, oligodontia, and odontodysplasia. Sebaceous nevi follow the lines of Blaschko and these can continue as linear intraoral lesions, as in mucosal papillomatosis.<ref>PMID:22683711</ref>

~~Authors~~: ~~Qamra~~, R., ~~Hubbard, S~~.R.

==Function==

[[http://www.uniprot.org/uniprot/GRB14_HUMAN GRB14_HUMAN]] Adapter protein which modulates coupling of cell surface receptor kinases with specific signaling pathways. Binds to, and suppresses signals from, the activated insulin receptor (INSR). Potent inhibitor of insulin-stimulated MAPK3 phosphorylation. Plays a critical role regulating PDPK1 membrane translocation in response to insulin stimulation and serves as an adapter protein to recruit PDPK1 to activated insulin receptor, thus promoting PKB/AKT1 phosphorylation and transduction of the insulin signal.<ref>PMID:15210700</ref> <ref>PMID:19648926</ref> [[http://www.uniprot.org/uniprot/RASH_HUMAN RASH_HUMAN]] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.<ref>PMID:14500341</ref> <ref>PMID:9020151</ref> <ref>PMID:12740440</ref>

~~Description~~: ~~Crystal structure of the Grb14 RA~~ and ~~PH domains in complex with GTP~~-~~loaded H-Ras~~

==About this Structure==

[[4k81]] is a 8 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Zasmidium_angulare Zasmidium angulare]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4K81 OCA].

==Reference==

[[Category: Homo sapiens]]

[[Category: Zasmidium angulare]]

[[Category: Hubbard, S R.]]

[[Category: Qamra, R.]]

[[Category: Adaptor protein]]

[[Category: Signaling protein]]

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@@ Line 1: / Line 1: @@
-'''Unreleased structure'''
+{{STRUCTURE_4k81|  PDB=4k81  |  SCENE=  }}
+===Crystal structure of the Grb14 RA and PH domains in complex with GTP-loaded H-Ras===
+{{ABSTRACT_PUBMED_23967305}}
-The entry 4k81 is ON HOLD  until Paper Publication
+==Disease==
+[[http://www.uniprot.org/uniprot/RASH_HUMAN RASH_HUMAN]] Defects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS) [MIM:[http://omim.org/entry/218040 218040]]. A rare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities (typically pulmonic stenosis, hypertrophic cardiomyopathy and/or atrial tachycardia), tumor predisposition, skin and musculoskeletal abnormalities.<ref>PMID:16170316</ref> <ref>PMID:16329078</ref> <ref>PMID:16443854</ref> <ref>PMID:17054105</ref> <ref>PMID:18247425</ref> <ref>PMID:18039947</ref> <ref>PMID:19995790</ref>   Defects in HRAS are the cause of congenital myopathy with excess of muscle spindles (CMEMS) [MIM:[http://omim.org/entry/218040 218040]]. CMEMS is a variant of Costello syndrome.<ref>PMID:17412879</ref>   Defects in HRAS may be a cause of susceptibility to Hurthle cell thyroid carcinoma (HCTC) [MIM:[http://omim.org/entry/607464 607464]]. Hurthle cell thyroid carcinoma accounts for approximately 3% of all thyroid cancers. Although they are classified as variants of follicular neoplasms, they are more often multifocal and somewhat more aggressive and are less likely to take up iodine than are other follicular neoplasms.  Note=Mutations which change positions 12, 13 or 61 activate the potential of HRAS to transform cultured cells and are implicated in a variety of human tumors.  Defects in HRAS are a cause of susceptibility to bladder cancer (BLC) [MIM:[http://omim.org/entry/109800 109800]]. A malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and at different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin, flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences.  Note=Defects in HRAS are the cause of oral squamous cell carcinoma (OSCC).<ref>PMID:1459726</ref>   Defects in HRAS are the cause of Schimmelpenning-Feuerstein-Mims syndrome (SFM) [MIM:[http://omim.org/entry/163200 163200]]. A disease characterized by sebaceous nevi, often on the face, associated with variable ipsilateral abnormalities of the central nervous system, ocular anomalies, and skeletal defects. Many oral manifestations have been reported, not only including hypoplastic and malformed teeth, and mucosal papillomatosis, but also ankyloglossia, hemihyperplastic tongue, intraoral nevus, giant cell granuloma, ameloblastoma, bone cysts, follicular cysts, oligodontia, and odontodysplasia. Sebaceous nevi follow the lines of Blaschko and these can continue as linear intraoral lesions, as in mucosal papillomatosis.<ref>PMID:22683711</ref>
-Authors: Qamra, R., Hubbard, S.R.
+==Function==
+[[http://www.uniprot.org/uniprot/GRB14_HUMAN GRB14_HUMAN]] Adapter protein which modulates coupling of cell surface receptor kinases with specific signaling pathways. Binds to, and suppresses signals from, the activated insulin receptor (INSR). Potent inhibitor of insulin-stimulated MAPK3 phosphorylation. Plays a critical role regulating PDPK1 membrane translocation in response to insulin stimulation and serves as an adapter protein to recruit PDPK1 to activated insulin receptor, thus promoting PKB/AKT1 phosphorylation and transduction of the insulin signal.<ref>PMID:15210700</ref> <ref>PMID:19648926</ref>  [[http://www.uniprot.org/uniprot/RASH_HUMAN RASH_HUMAN]] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.<ref>PMID:14500341</ref> <ref>PMID:9020151</ref> <ref>PMID:12740440</ref>
-Description: Crystal structure of the Grb14 RA and PH domains in complex with GTP-loaded H-Ras
+==About this Structure==
+[[4k81]] is a 8 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Zasmidium_angulare Zasmidium angulare]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4K81 OCA].
+==Reference==
+<ref group="xtra">PMID:023967305</ref><references group="xtra"/><references/>
+[[Category: Homo sapiens]]
+[[Category: Zasmidium angulare]]
+[[Category: Hubbard, S R.]]
+[[Category: Qamra, R.]]
+[[Category: Adaptor protein]]
+[[Category: Signaling protein]]