1txq: Difference between revisions

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-{{Seed}}
-[[Image:1txq.png|left|200px]]
-<!--
+==Crystal structure of the EB1 C-terminal domain complexed with the CAP-Gly domain of p150Glued==
-The line below this paragraph, containing "STRUCTURE_1txq", creates the "Structure Box" on the page.
+<StructureSection load='1txq' size='340' side='right'caption='[[1txq]], [[Resolution|resolution]] 1.80&Aring;' scene=''>
-You may change the PDB parameter (which sets the PDB file loaded into the applet)
+== Structural highlights ==
-or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
+<table><tr><td colspan='2'>[[1txq]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TXQ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1TXQ FirstGlance]. <br>
-or leave the SCENE parameter empty for the default display.
+</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.8&#8491;</td></tr>
--->
+<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=1txq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1txq OCA], [https://pdbe.org/1txq PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1txq RCSB], [https://www.ebi.ac.uk/pdbsum/1txq PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1txq ProSAT]</span></td></tr>
-{{STRUCTURE_1txq|  PDB=1txq  |  SCENE=  }}
+</table>
+== Disease ==
+[https://www.uniprot.org/uniprot/DCTN1_HUMAN DCTN1_HUMAN] Defects in DCTN1 are the cause of distal hereditary motor neuronopathy type 7B (HMN7B) [MIM:[https://omim.org/entry/607641 607641]; also known as progressive lower motor neuron disease (PLMND). HMN7B is a neuromuscular disorder. Distal hereditary motor neuronopathies constitute a heterogeneous group of neuromuscular disorders caused by selective degeneration of motor neurons in the anterior horn of the spinal cord, without sensory deficit in the posterior horn. The overall clinical picture consists of a classical distal muscular atrophy syndrome in the legs without clinical sensory loss. The disease starts with weakness and wasting of distal muscles of the anterior tibial and peroneal compartments of the legs. Later on, weakness and atrophy may expand to the proximal muscles of the lower limbs and/or to the distal upper limbs.<ref>PMID:12627231</ref> <ref>PMID:16505168</ref> <ref>PMID:19136952</ref> <ref>PMID:19279216</ref>   Defects in DCTN1 are a cause of susceptibility to amyotrophic lateral sclerosis (ALS) [MIM:[https://omim.org/entry/105400 105400]. ALS is a neurodegenerative disorder affecting upper and lower motor neurons, and resulting in fatal paralysis. Sensory abnormalities are absent. Death usually occurs within 2 to 5 years. The etiology is likely to be multifactorial, involving both genetic and environmental factors.<ref>PMID:15326253</ref> <ref>PMID:16240349</ref>   Defects in DCTN1 are the cause of Perry syndrome (PERRYS) [MIM:[https://omim.org/entry/168605 168605]; also called parkinsonism with alveolar hypoventilation and mental depression. Perry syndrome is a neuropsychiatric disorder characterized by mental depression not responsive to antidepressant drugs or electroconvulsive therapy, sleep disturbances, exhaustion and marked weight loss. Parkinsonism develops later and respiratory failure occurred terminally.<ref>PMID:19136952</ref>
+== Function ==
+[https://www.uniprot.org/uniprot/DCTN1_HUMAN DCTN1_HUMAN] Required for the cytoplasmic dynein-driven retrograde movement of vesicles and organelles along microtubules. Dynein-dynactin interaction is a key component of the mechanism of axonal transport of vesicles and organelles.
+== Evolutionary Conservation ==
+[[Image:Consurf_key_small.gif|200px|right]]
+Check<jmol>
+  <jmolCheckbox>
+    <scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/tx/1txq_consurf.spt"</scriptWhenChecked>
+    <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
+    <text>to colour the structure by Evolutionary Conservation</text>
+  </jmolCheckbox>
+</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=1txq ConSurf].
+<div style="clear:both"></div>
-===Crystal structure of the EB1 C-terminal domain complexed with the CAP-Gly domain of p150Glued===
+==See Also==
+*[[Dynactin|Dynactin]]
+*[[End-binding protein|End-binding protein]]
-<!--
+*[[Microtubule-associated protein 3D structures|Microtubule-associated protein 3D structures]]
-The line below this paragraph, {{ABSTRACT_PUBMED_16109370}}, adds the Publication Abstract to the page
+== References ==
-(as it appears on PubMed at http://www.pubmed.gov), where 16109370 is the PubMed ID number.
+<references/>
--->
+__TOC__
-{{ABSTRACT_PUBMED_16109370}}
+</StructureSection>
-==About this Structure==
-TXQ is a [[Protein complex]] structure of sequences from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1TXQ OCA].
-==Reference==
-Structural basis for the activation of microtubule assembly by the EB1 and p150Glued complex., Hayashi I, Wilde A, Mal TK, Ikura M, Mol Cell. 2005 Aug 19;19(4):449-60. PMID:[http://www.ncbi.nlm.nih.gov/pubmed/16109370 16109370]
 [[Category: Homo sapiens]]
-[[Category: Protein complex]]
+[[Category: Large Structures]]
-[[Category: Hayashi, I.]]
+[[Category: Hayashi I]]
-[[Category: Ikura, M.]]
+[[Category: Ikura M]]
-[[Category: Protein complex]]
-''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Mon Jul 28 00:06:28 2008''