2hl3: Difference between revisions

← Older edit

Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)

OCA

@@ Line 3: / Line 3: @@
 <StructureSection load='2hl3' size='340' side='right'caption='[[2hl3]], [[Resolution|resolution]] 2.03&Aring;' scene=''>
 == Structural highlights ==
-<table><tr><td colspan='2'>[[2hl3]] is a 3 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2HL3 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2HL3 FirstGlance]. <br>
+<table><tr><td colspan='2'>[[2hl3]] is a 3 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=2HL3 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2HL3 FirstGlance]. <br>
-</td></tr><tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[2coy|2coy]], [[1txq|1txq]], [[2hkn|2hkn]], [[2hl5|2hl5]]</div></td></tr>
+</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.03&#8491;</td></tr>
-<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">DCTN1 ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=2hl3 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2hl3 OCA], [https://pdbe.org/2hl3 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2hl3 RCSB], [https://www.ebi.ac.uk/pdbsum/2hl3 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2hl3 ProSAT]</span></td></tr>
 </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>
+[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. [[https://www.uniprot.org/uniprot/MARE1_HUMAN MARE1_HUMAN]] Binds to the plus end of microtubules and regulates the dynamics of the microtubule cytoskeleton. Promotes cytoplasmic microtubule nucleation and elongation. May be involved in spindle function by stabilizing microtubules and anchoring them at centrosomes. May play a role in cell migration.<ref>PMID:12388762</ref> <ref>PMID:21646404</ref> <ref>PMID:16109370</ref> <ref>PMID:19632184</ref>
+[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]]
@@ Line 22: / Line 21: @@
 </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=2hl3 ConSurf].
 <div style="clear:both"></div>
-<div style="background-color:#fffaf0;">
-== Publication Abstract from PubMed ==
-Dynamic microtubule plus-end tracking protein (+TIP) networks are implicated in all functions of microtubules, but the molecular determinants of their interactions are largely unknown. Here, we have explored key binding modes of +TIPs by analyzing the interactions between selected CAP-Gly, EB-like, and carboxy-terminal EEY/F-COO(-) sequence motifs. X-ray crystallography and biophysical binding studies demonstrate that the beta2-beta3 loop of CAP-Gly domains determines EB-like motif binding specificity. They further show how CAP-Gly domains serve as recognition domains for EEY/F-COO(-) motifs, which represent characteristic and functionally important sequence elements in EB, CLIP-170, and alpha-tubulin. Our findings provide a molecular basis for understanding the modular interaction modes between alpha-tubulin, CLIPs, EB proteins, and the dynactin-dynein motor complex and suggest that multiple low-affinity binding sites in different combinations control dynamic +TIP networks at microtubule ends. They further offer insights into the structural consequences of genetic CAP-Gly domain defects found in severe human disorders.
-Key interaction modes of dynamic +TIP networks.,Honnappa S, Okhrimenko O, Jaussi R, Jawhari H, Jelesarov I, Winkler FK, Steinmetz MO Mol Cell. 2006 Sep 1;23(5):663-71. PMID:16949363<ref>PMID:16949363</ref>
-From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
-</div>
-<div class="pdbe-citations 2hl3" style="background-color:#fffaf0;"></div>
 ==See Also==
@@ Line 38: / Line 28: @@
 __TOC__
 </StructureSection>
-[[Category: Human]]
+[[Category: Homo sapiens]]
 [[Category: Large Structures]]
-[[Category: Honnappa, S]]
+[[Category: Honnappa S]]
-[[Category: Steinmetz, M O]]
+[[Category: Steinmetz MO]]
-[[Category: Winkler, F K]]
+[[Category: Winkler FK]]
-[[Category: Tip protein complex structure]]
-[[Category: Alpha-tubulin]]
-[[Category: Clip-170]]
-[[Category: Cytoskeleton associated protein]]
-[[Category: Dynactin]]
-[[Category: Eb1]]
-[[Category: Eey/f-coo- sequence motif]]
-[[Category: Microtubule binding]]
-[[Category: P150glued]]
-[[Category: Structural protein]]