4cc0: Difference between revisions

Line 1:

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

===Notch ligand, Jagged-1, contains an N-terminal C2 domain===

~~The~~ entry ~~4cc0~~ is ~~ON HOLD~~ ~~until Paper Publication~~

==Disease==

[[http://www.uniprot.org/uniprot/JAG1_HUMAN JAG1_HUMAN]] Defects in JAG1 are the cause of Alagille syndrome type 1 (ALGS1) [MIM:[http://omim.org/entry/118450 118450]]. Alagille syndrome is an autosomal dominant multisystem disorder defined clinically by hepatic bile duct paucity and cholestasis in association with cardiac, skeletal, and ophthalmologic manifestations. There are characteristic facial features and less frequent clinical involvement of the renal and vascular systems.<ref>PMID:9207788</ref> <ref>PMID:9207787</ref> <ref>PMID:9585603</ref> <ref>PMID:10220506</ref> <ref>PMID:10533065</ref> <ref>PMID:11058898</ref> <ref>PMID:11157803</ref> <ref>PMID:11139247</ref> <ref>PMID:11180599</ref> <ref>PMID:12442286</ref> <ref>PMID:12497640</ref> <ref>PMID:15712272</ref> <ref>PMID:16575836</ref> Defects in JAG1 are a cause of tetralogy of Fallot (TOF) [MIM:[http://omim.org/entry/187500 187500]]. TOF is a congenital heart anomaly which consists of pulmonary stenosis, ventricular septal defect, dextroposition of the aorta (aorta is on the right side instead of the left) and hypertrophy of the right ventricle. This condition results in a blue baby at birth due to inadequate oxygenation. Surgical correction is emergent.<ref>PMID:9207787</ref> <ref>PMID:11152664</ref>

~~Authors~~: ~~Chilakuri, C~~.~~, Sheppard, D~~.~~, Ilagan, M~~.~~, Holt, L~~.~~, Abbott, F~~.~~, Liang, S~~.~~, Kopan, R., Handford, P., Lea, S~~.

==Function==

[[http://www.uniprot.org/uniprot/JAG1_HUMAN JAG1_HUMAN]] Ligand for multiple Notch receptors and involved in the mediation of Notch signaling. May be involved in cell-fate decisions during hematopoiesis. Seems to be involved in early and late stages of mammalian cardiovascular development. Inhibits myoblast differentiation (By similarity). Enhances fibroblast growth factor-induced angiogenesis (in vitro).<ref>PMID:9462510</ref> <ref>PMID:18660822</ref>

~~Description~~: ~~Notch ligand~~, ~~Jagged-1~~, ~~contains an N~~-~~terminal C2~~ domain

==About this Structure==

[[4cc0]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4CC0 OCA].

==Reference==

[[Category: Abbott, F.]]

[[Category: Chilakuri, C R.]]

[[Category: Handford, P A.]]

[[Category: Holt, L R.]]

[[Category: Ilagan, M X.G.]]

[[Category: Kopan, R.]]

[[Category: Lea, S M.]]

[[Category: Liang, S.]]

[[Category: Sheppard, D.]]

[[Category: Developmental protein]]

[[Category: Disease mutation]]

[[Category: Dsl]]

[[Category: Egf]]

[[Category: Egf-like domain]]

[[Category: Extracellular]]

[[Category: Glycoprotein]]

[[Category: Lipid]]

[[Category: Membrane]]

[[Category: Notch signaling pathway]]

[[Category: Protein-binding]]

[[Category: Signaling protein]]

[[Category: Signalling]]

[[Category: Transmembrane]]

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@@ Line 1: / Line 1: @@
-'''Unreleased structure'''
+{{STRUCTURE_4cc0|  PDB=4cc0  |  SCENE=  }}
+===Notch ligand, Jagged-1, contains an N-terminal C2 domain===
-The entry 4cc0 is ON HOLD  until Paper Publication
+==Disease==
+[[http://www.uniprot.org/uniprot/JAG1_HUMAN JAG1_HUMAN]] Defects in JAG1 are the cause of Alagille syndrome type 1 (ALGS1) [MIM:[http://omim.org/entry/118450 118450]]. Alagille syndrome is an autosomal dominant multisystem disorder defined clinically by hepatic bile duct paucity and cholestasis in association with cardiac, skeletal, and ophthalmologic manifestations. There are characteristic facial features and less frequent clinical involvement of the renal and vascular systems.<ref>PMID:9207788</ref> <ref>PMID:9207787</ref> <ref>PMID:9585603</ref> <ref>PMID:10220506</ref> <ref>PMID:10533065</ref> <ref>PMID:11058898</ref> <ref>PMID:11157803</ref> <ref>PMID:11139247</ref> <ref>PMID:11180599</ref> <ref>PMID:12442286</ref> <ref>PMID:12497640</ref> <ref>PMID:15712272</ref> <ref>PMID:16575836</ref>   Defects in JAG1 are a cause of tetralogy of Fallot (TOF) [MIM:[http://omim.org/entry/187500 187500]]. TOF is a congenital heart anomaly which consists of pulmonary stenosis, ventricular septal defect, dextroposition of the aorta (aorta is on the right side instead of the left) and hypertrophy of the right ventricle. This condition results in a blue baby at birth due to inadequate oxygenation. Surgical correction is emergent.<ref>PMID:9207787</ref> <ref>PMID:11152664</ref>
-Authors: Chilakuri, C., Sheppard, D., Ilagan, M., Holt, L., Abbott, F., Liang, S., Kopan, R., Handford, P., Lea, S.
+==Function==
+[[http://www.uniprot.org/uniprot/JAG1_HUMAN JAG1_HUMAN]] Ligand for multiple Notch receptors and involved in the mediation of Notch signaling. May be involved in cell-fate decisions during hematopoiesis. Seems to be involved in early and late stages of mammalian cardiovascular development. Inhibits myoblast differentiation (By similarity). Enhances fibroblast growth factor-induced angiogenesis (in vitro).<ref>PMID:9462510</ref> <ref>PMID:18660822</ref>
-Description: Notch ligand, Jagged-1, contains an N-terminal C2 domain
+==About this Structure==
+[[4cc0]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4CC0 OCA].
+==Reference==
+<references group="xtra"/><references/>
+[[Category: Abbott, F.]]
+[[Category: Chilakuri, C R.]]
+[[Category: Handford, P A.]]
+[[Category: Holt, L R.]]
+[[Category: Ilagan, M X.G.]]
+[[Category: Kopan, R.]]
+[[Category: Lea, S M.]]
+[[Category: Liang, S.]]
+[[Category: Sheppard, D.]]
+[[Category: Developmental protein]]
+[[Category: Disease mutation]]
+[[Category: Dsl]]
+[[Category: Egf]]
+[[Category: Egf-like domain]]
+[[Category: Extracellular]]
+[[Category: Glycoprotein]]
+[[Category: Lipid]]
+[[Category: Membrane]]
+[[Category: Notch signaling pathway]]
+[[Category: Protein-binding]]
+[[Category: Signaling protein]]
+[[Category: Signalling]]
+[[Category: Transmembrane]]