5tfg - Revision history

OCA at 12:59, 4 October 2023

OCA — Wed, 04 Oct 2023 12:59:30 GMT

←Older revision		Revision as of 12:59, 4 October 2023
Line 3:		Line 3:
	<StructureSection load='5tfg' size='340' side='right'caption='[[5tfg]], [[Resolution\|resolution]] 1.91Å' scene=''>		<StructureSection load='5tfg' size='340' side='right'caption='[[5tfg]], [[Resolution\|resolution]] 1.91Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5tfg]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5TFG OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=5TFG FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5tfg]] is a 1 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=5TFG OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5TFG FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=M5T:5~~-~~Methyluridine+triphosphate'>M5T</scene>~~, ~~<scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>~~</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]] 1.91Å</td></tr>
-	<tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat"~~>[[5tf7\|5tf7]], [[5tf8\|5tf8]], [[5tfa\|5tfa]], [[5tfb\|5tfb]], [[5tfc\|5tfc]], [[5tfd\|5tfd]], [[5tfe\|5tfe]], [[5tff\|5tff]], [[5tfh\|5tfh]], [[5tfi\|5tfi]], [[5tfj\|5tfj]], [[5tgk\|5tgk]]</td></tr>~~	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=M5T:5-Methyluridine+triphosphate'>M5T</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>
-	~~<tr~~ id~~='activity'><td class~~="~~sblockLbl~~"><~~b>Activity~~:~~</b~~></td><~~td class~~=~~"sblockDat"><span class~~=~~'plainlinks~~'>[http://en.wikipedia.org/wiki/Channel-conductance-controlling_ATPase Channel-conductance-controlling ATPase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.6.3.49 3.6.3.49] </~~span~~></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=5tfg FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5tfg OCA], [https://pdbe.org/5tfg PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5tfg RCSB], [https://www.ebi.ac.uk/pdbsum/5tfg PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5tfg ProSAT]</span></td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://proteopedia.org/fgij/fg.htm?mol=5tfg FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5tfg OCA], [~~http~~://pdbe.org/5tfg PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=5tfg RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/5tfg PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=5tfg ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/CFTR_HUMAN CFTR_HUMAN]] Defects in CFTR are the cause of cystic fibrosis (CF) [MIM:[~~http~~://omim.org/entry/219700 219700]]; also known as mucoviscidosis. CF is the most common genetic disease in the Caucasian population, with a prevalence of about 1 in 2'000 live births. Inheritance is autosomal recessive. CF is a common generalized disorder of exocrine gland function which impairs clearance of secretions in a variety of organs. It is characterized by the triad of chronic bronchopulmonary disease (with recurrent respiratory infections), pancreatic insufficiency (which leads to malabsorption and growth retardation) and elevated sweat electrolytes.<ref>PMID:1695717</ref> <ref>PMID:2236053</ref> <ref>PMID:1710600</ref> <ref>PMID:1284466</ref> <ref>PMID:1284468</ref> <ref>PMID:1284530</ref> <ref>PMID:1284529</ref> <ref>PMID:7680525</ref> <ref>PMID:7683628</ref> <ref>PMID:7683954</ref> <ref>PMID:7505694</ref> <ref>PMID:7504969</ref> <ref>PMID:7522211</ref> <ref>PMID:7513296</ref> <ref>PMID:7525450</ref> <ref>PMID:7520022</ref> <ref>PMID:7524913</ref> <ref>PMID:7524909</ref> <ref>PMID:7517264</ref> <ref>PMID:8081395</ref> <ref>PMID:7544319</ref> <ref>PMID:8522333</ref> <ref>PMID:7537150</ref> <ref>PMID:7541273</ref> <ref>PMID:7581407</ref> <ref>PMID:7543567</ref> <ref>PMID:7541510</ref> <ref>PMID:8800923</ref> <ref>PMID:8829633</ref> <ref>PMID:8723693</ref> <ref>PMID:8723695</ref> <ref>PMID:8956039</ref> <ref>PMID:9101301</ref> <ref>PMID:9222768</ref> <ref>PMID:9375855</ref> <ref>PMID:9401006</ref> <ref>PMID:9443874</ref> <ref>PMID:9521595</ref> <ref>PMID:9921909</ref> <ref>PMID:9736778</ref> <ref>PMID:9482579</ref> <ref>PMID:9554753</ref> <ref>PMID:9452048</ref> <ref>PMID:9452054</ref> <ref>PMID:9452073</ref> <ref>PMID:10094564</ref> Defects in CFTR are the cause of congenital bilateral absence of the vas deferens (CBAVD) [MIM:[~~http~~://omim.org/entry/277180 277180]]. CBAVD is an important cause of sterility in men and could represent an incomplete form of cystic fibrosis, as the majority of men suffering from cystic fibrosis lack the vas deferens.<ref>PMID:7529962</ref> <ref>PMID:7539342</ref> <ref>PMID:9067761</ref> <ref>PMID:10651488</ref> [:]	+	[https://www.uniprot.org/uniprot/CFTR_HUMAN CFTR_HUMAN] Defects in CFTR are the cause of cystic fibrosis (CF) [MIM:[https://omim.org/entry/219700 219700]; also known as mucoviscidosis. CF is the most common genetic disease in the Caucasian population, with a prevalence of about 1 in 2'000 live births. Inheritance is autosomal recessive. CF is a common generalized disorder of exocrine gland function which impairs clearance of secretions in a variety of organs. It is characterized by the triad of chronic bronchopulmonary disease (with recurrent respiratory infections), pancreatic insufficiency (which leads to malabsorption and growth retardation) and elevated sweat electrolytes.<ref>PMID:1695717</ref> <ref>PMID:2236053</ref> <ref>PMID:1710600</ref> <ref>PMID:1284466</ref> <ref>PMID:1284468</ref> <ref>PMID:1284530</ref> <ref>PMID:1284529</ref> <ref>PMID:7680525</ref> <ref>PMID:7683628</ref> <ref>PMID:7683954</ref> <ref>PMID:7505694</ref> <ref>PMID:7504969</ref> <ref>PMID:7522211</ref> <ref>PMID:7513296</ref> <ref>PMID:7525450</ref> <ref>PMID:7520022</ref> <ref>PMID:7524913</ref> <ref>PMID:7524909</ref> <ref>PMID:7517264</ref> <ref>PMID:8081395</ref> <ref>PMID:7544319</ref> <ref>PMID:8522333</ref> <ref>PMID:7537150</ref> <ref>PMID:7541273</ref> <ref>PMID:7581407</ref> <ref>PMID:7543567</ref> <ref>PMID:7541510</ref> <ref>PMID:8800923</ref> <ref>PMID:8829633</ref> <ref>PMID:8723693</ref> <ref>PMID:8723695</ref> <ref>PMID:8956039</ref> <ref>PMID:9101301</ref> <ref>PMID:9222768</ref> <ref>PMID:9375855</ref> <ref>PMID:9401006</ref> <ref>PMID:9443874</ref> <ref>PMID:9521595</ref> <ref>PMID:9921909</ref> <ref>PMID:9736778</ref> <ref>PMID:9482579</ref> <ref>PMID:9554753</ref> <ref>PMID:9452048</ref> <ref>PMID:9452054</ref> <ref>PMID:9452073</ref> <ref>PMID:10094564</ref> Defects in CFTR are the cause of congenital bilateral absence of the vas deferens (CBAVD) [MIM:[https://omim.org/entry/277180 277180]. CBAVD is an important cause of sterility in men and could represent an incomplete form of cystic fibrosis, as the majority of men suffering from cystic fibrosis lack the vas deferens.<ref>PMID:7529962</ref> <ref>PMID:7539342</ref> <ref>PMID:9067761</ref> <ref>PMID:10651488</ref> [:]
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/CFTR_HUMAN CFTR_HUMAN]] Involved in the transport of chloride ions. May regulate bicarbonate secretion and salvage in epithelial cells by regulating the SLC4A7 transporter. Can inhibit the chloride channel activity of ANO1.<ref>PMID:22178883</ref>	+	[https://www.uniprot.org/uniprot/CFTR_HUMAN CFTR_HUMAN] Involved in the transport of chloride ions. May regulate bicarbonate secretion and salvage in epithelial cells by regulating the SLC4A7 transporter. Can inhibit the chloride channel activity of ANO1.<ref>PMID:22178883</ref>

	==See Also==		==See Also==
Line 20:		Line 19:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Channel-conductance-controlling ATPase~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Aleksandrov~~, A A~~]]	+	[[Category: Aleksandrov AA]]
-	[[Category: An, J]]	+	[[Category: An J]]
-	[[Category: Boel, G]]	+	[[Category: Boel G]]
-	[[Category: Brouillette~~, C G~~]]	+	[[Category: Brouillette CG]]
-	[[Category: Dokholyan~~, N V~~]]	+	[[Category: Dokholyan NV]]
-	[[Category: Forouhar, F]]	+	[[Category: Forouhar F]]
-	[[Category: Hunt~~, J F~~]]	+	[[Category: Hunt JF]]
-	[[Category: Kaplan, A]]	+	[[Category: Kaplan A]]
-	[[Category: Khazanov, N]]	+	[[Category: Khazanov N]]
-	[[Category: Kota, P]]	+	[[Category: Kota P]]
-	[[Category: Proctor, E]]	+	[[Category: Proctor E]]
-	[[Category: Riordan~~, J R~~]]	+	[[Category: Riordan JR]]
-	[[Category: Senderowitz, H]]	+	[[Category: Senderowitz H]]
-	[[Category: Stockwell~~, B R~~]]	+	[[Category: Stockwell BR]]
-	[[Category: Wang, C]]	+	[[Category: Wang C]]
-	[[Category: Yang, Z]]	+	[[Category: Yang Z]]
-	~~[[Category: Abc transport]]~~	+
-	~~[[Category: Atp]]~~	+
-	~~[[Category: Cftr]]~~	+
-	~~[[Category: Hnbd1]]~~	+
-	~~[[Category: Hydrolase~~]]	+

OCA at 12:09, 23 September 2020

OCA — Wed, 23 Sep 2020 12:09:04 GMT

←Older revision		Revision as of 12:09, 23 September 2020
Line 1:		Line 1:

	==Nucleotide-binding domain 1 of the human cystic fibrosis transmembrane conductance regulator (CFTR) with 5-methyl-UTP==		==Nucleotide-binding domain 1 of the human cystic fibrosis transmembrane conductance regulator (CFTR) with 5-methyl-UTP==
-	<StructureSection load='5tfg' size='340' side='right' caption='[[5tfg]], [[Resolution\|resolution]] 1.91Å' scene=''>	+	<StructureSection load='5tfg' size='340' side='right'caption='[[5tfg]], [[Resolution\|resolution]] 1.91Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5tfg]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5TFG OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5TFG FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5tfg]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5TFG OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=5TFG FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=M5T:5-Methyluridine+triphosphate'>M5T</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=M5T:5-Methyluridine+triphosphate'>M5T</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5tf7\|5tf7]], [[5tf8\|5tf8]], [[5tfa\|5tfa]], [[5tfb\|5tfb]], [[5tfc\|5tfc]], [[5tfd\|5tfd]], [[5tfe\|5tfe]], [[5tff\|5tff]], [[5tfh\|5tfh]], [[5tfi\|5tfi]], [[5tfj\|5tfj]], [[5tgk\|5tgk]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5tf7\|5tf7]], [[5tf8\|5tf8]], [[5tfa\|5tfa]], [[5tfb\|5tfb]], [[5tfc\|5tfc]], [[5tfd\|5tfd]], [[5tfe\|5tfe]], [[5tff\|5tff]], [[5tfh\|5tfh]], [[5tfi\|5tfi]], [[5tfj\|5tfj]], [[5tgk\|5tgk]]</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Channel-conductance-controlling_ATPase Channel-conductance-controlling ATPase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.6.3.49 3.6.3.49] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Channel-conductance-controlling_ATPase Channel-conductance-controlling ATPase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.6.3.49 3.6.3.49] </span></td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5tfg FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5tfg OCA], [http://pdbe.org/5tfg PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5tfg RCSB], [http://www.ebi.ac.uk/pdbsum/5tfg PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5tfg ProSAT]</span></td></tr>	+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=5tfg FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5tfg OCA], [http://pdbe.org/5tfg PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5tfg RCSB], [http://www.ebi.ac.uk/pdbsum/5tfg PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5tfg ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 13:		Line 13:
	== Function ==		== Function ==
	[[http://www.uniprot.org/uniprot/CFTR_HUMAN CFTR_HUMAN]] Involved in the transport of chloride ions. May regulate bicarbonate secretion and salvage in epithelial cells by regulating the SLC4A7 transporter. Can inhibit the chloride channel activity of ANO1.<ref>PMID:22178883</ref>		[[http://www.uniprot.org/uniprot/CFTR_HUMAN CFTR_HUMAN]] Involved in the transport of chloride ions. May regulate bicarbonate secretion and salvage in epithelial cells by regulating the SLC4A7 transporter. Can inhibit the chloride channel activity of ANO1.<ref>PMID:22178883</ref>
		+
		+	==See Also==
		+	*[[ABC transporter 3D structures\|ABC transporter 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
Line 18:		Line 21:
	</StructureSection>		</StructureSection>
	[[Category: Channel-conductance-controlling ATPase]]		[[Category: Channel-conductance-controlling ATPase]]
		+	[[Category: Large Structures]]
	[[Category: Aleksandrov, A A]]		[[Category: Aleksandrov, A A]]
	[[Category: An, J]]		[[Category: An, J]]

OCA at 06:10, 9 May 2018

OCA — Wed, 09 May 2018 06:10:15 GMT

←Older revision		Revision as of 06:10, 9 May 2018
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 5tfg is ~~ON HOLD~~ ~~until Apr 30 2019~~	+	==Nucleotide-binding domain 1 of the human cystic fibrosis transmembrane conductance regulator (CFTR) with 5-methyl-UTP==
-		+	<StructureSection load='5tfg' size='340' side='right' caption='[[5tfg]], [[Resolution\|resolution]] 1.91Å' scene=''>
-	~~Authors~~:	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[5tfg]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5TFG OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5TFG FirstGlance]. <br>
-	~~Description~~:	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=M5T:5-Methyluridine+triphosphate'>M5T</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr>
-	[[Category: ~~Unreleased Structures~~]]	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5tf7\|5tf7]], [[5tf8\|5tf8]], [[5tfa\|5tfa]], [[5tfb\|5tfb]], [[5tfc\|5tfc]], [[5tfd\|5tfd]], [[5tfe\|5tfe]], [[5tff\|5tff]], [[5tfh\|5tfh]], [[5tfi\|5tfi]], [[5tfj\|5tfj]], [[5tgk\|5tgk]]</td></tr>
		+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Channel-conductance-controlling_ATPase Channel-conductance-controlling ATPase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.6.3.49 3.6.3.49] </span></td></tr>
		+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5tfg FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5tfg OCA], [http://pdbe.org/5tfg PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5tfg RCSB], [http://www.ebi.ac.uk/pdbsum/5tfg PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5tfg ProSAT]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/CFTR_HUMAN CFTR_HUMAN]] Defects in CFTR are the cause of cystic fibrosis (CF) [MIM:[http://omim.org/entry/219700 219700]]; also known as mucoviscidosis. CF is the most common genetic disease in the Caucasian population, with a prevalence of about 1 in 2'000 live births. Inheritance is autosomal recessive. CF is a common generalized disorder of exocrine gland function which impairs clearance of secretions in a variety of organs. It is characterized by the triad of chronic bronchopulmonary disease (with recurrent respiratory infections), pancreatic insufficiency (which leads to malabsorption and growth retardation) and elevated sweat electrolytes.<ref>PMID:1695717</ref> <ref>PMID:2236053</ref> <ref>PMID:1710600</ref> <ref>PMID:1284466</ref> <ref>PMID:1284468</ref> <ref>PMID:1284530</ref> <ref>PMID:1284529</ref> <ref>PMID:7680525</ref> <ref>PMID:7683628</ref> <ref>PMID:7683954</ref> <ref>PMID:7505694</ref> <ref>PMID:7504969</ref> <ref>PMID:7522211</ref> <ref>PMID:7513296</ref> <ref>PMID:7525450</ref> <ref>PMID:7520022</ref> <ref>PMID:7524913</ref> <ref>PMID:7524909</ref> <ref>PMID:7517264</ref> <ref>PMID:8081395</ref> <ref>PMID:7544319</ref> <ref>PMID:8522333</ref> <ref>PMID:7537150</ref> <ref>PMID:7541273</ref> <ref>PMID:7581407</ref> <ref>PMID:7543567</ref> <ref>PMID:7541510</ref> <ref>PMID:8800923</ref> <ref>PMID:8829633</ref> <ref>PMID:8723693</ref> <ref>PMID:8723695</ref> <ref>PMID:8956039</ref> <ref>PMID:9101301</ref> <ref>PMID:9222768</ref> <ref>PMID:9375855</ref> <ref>PMID:9401006</ref> <ref>PMID:9443874</ref> <ref>PMID:9521595</ref> <ref>PMID:9921909</ref> <ref>PMID:9736778</ref> <ref>PMID:9482579</ref> <ref>PMID:9554753</ref> <ref>PMID:9452048</ref> <ref>PMID:9452054</ref> <ref>PMID:9452073</ref> <ref>PMID:10094564</ref> Defects in CFTR are the cause of congenital bilateral absence of the vas deferens (CBAVD) [MIM:[http://omim.org/entry/277180 277180]]. CBAVD is an important cause of sterility in men and could represent an incomplete form of cystic fibrosis, as the majority of men suffering from cystic fibrosis lack the vas deferens.<ref>PMID:7529962</ref> <ref>PMID:7539342</ref> <ref>PMID:9067761</ref> <ref>PMID:10651488</ref> [:]
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/CFTR_HUMAN CFTR_HUMAN]] Involved in the transport of chloride ions. May regulate bicarbonate secretion and salvage in epithelial cells by regulating the SLC4A7 transporter. Can inhibit the chloride channel activity of ANO1.<ref>PMID:22178883</ref>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Channel-conductance-controlling ATPase]]
		+	[[Category: Aleksandrov, A A]]
		+	[[Category: An, J]]
		+	[[Category: Boel, G]]
		+	[[Category: Brouillette, C G]]
		+	[[Category: Dokholyan, N V]]
		+	[[Category: Forouhar, F]]
		+	[[Category: Hunt, J F]]
		+	[[Category: Kaplan, A]]
		+	[[Category: Khazanov, N]]
		+	[[Category: Kota, P]]
		+	[[Category: Proctor, E]]
		+	[[Category: Riordan, J R]]
		+	[[Category: Senderowitz, H]]
		+	[[Category: Stockwell, B R]]
		+	[[Category: Wang, C]]
		+	[[Category: Yang, Z]]
		+	[[Category: Abc transport]]
		+	[[Category: Atp]]
		+	[[Category: Cftr]]
		+	[[Category: Hnbd1]]
		+	[[Category: Hydrolase]]

OCA at 05:06, 28 March 2018

OCA — Wed, 28 Mar 2018 05:06:05 GMT

←Older revision		Revision as of 05:06, 28 March 2018
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 5tfg is ON HOLD until ~~Mar 25~~ 2019	+	The entry 5tfg is ON HOLD until Apr 30 2019

	Authors:		Authors:

OCA at 04:41, 1 November 2017

OCA — Wed, 01 Nov 2017 04:41:44 GMT

←Older revision		Revision as of 04:41, 1 November 2017
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 5tfg is ON HOLD until ~~Nov 24 2018~~	+	The entry 5tfg is ON HOLD until Mar 25 2019

	Authors:		Authors:

OCA at 13:22, 27 September 2017

OCA — Wed, 27 Sep 2017 13:22:19 GMT

←Older revision		Revision as of 13:22, 27 September 2017
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 5tfg is ON HOLD until ~~Sep 25~~ 2018	+	The entry 5tfg is ON HOLD until Nov 24 2018

	Authors:		Authors:

OCA at 17:00, 26 October 2016

OCA — Wed, 26 Oct 2016 17:00:35 GMT

←Older revision		Revision as of 17:00, 26 October 2016
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 5tfg is ON HOLD	+	The entry 5tfg is ON HOLD until Sep 25 2018

	Authors:		Authors:

OCA: Protected "5tfg" [edit=sysop:move=sysop]

OCA — Wed, 05 Oct 2016 20:00:43 GMT

Protected "5tfg" [edit=sysop:move=sysop]

←Older revision

Revision as of 20:00, 5 October 2016

OCA: New page: '''Unreleased structure''' The entry 5tfg is ON HOLD Authors: Description: Category: Unreleased Structures

OCA — Wed, 05 Oct 2016 20:00:42 GMT

New page: '''Unreleased structure''' The entry 5tfg is ON HOLD Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 5tfg is ON HOLD

Authors:

Description:
[[Category: Unreleased Structures]]