6k9l - Revision history

OCA at 10:41, 27 March 2024

OCA — Wed, 27 Mar 2024 10:41:56 GMT

←Older revision		Revision as of 10:41, 27 March 2024
Line 3:		Line 3:
	<SX load='6k9l' size='340' side='right' viewer='molstar' caption='[[6k9l]], [[Resolution\|resolution]] 4.27Å' scene=''>		<SX load='6k9l' size='340' side='right' viewer='molstar' caption='[[6k9l]], [[Resolution\|resolution]] 4.27Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6k9l]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6K9L OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=6K9L FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6k9l]] 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=6K9L OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6K9L FirstGlance]. <br>
-	</td></tr><tr id='~~activity~~'><td class="sblockLbl"><b>~~Activity~~:</b></td><td class="sblockDat"~~><span class~~=~~'plainlinks'~~>[~~http://en.wikipedia.org/wiki/Non-specific_serine/threonine_protein_kinase Non-specific serine/threonine protein kinase~~]~~, with EC number [http://www~~.~~brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.1 2.7.11.1] </span>~~</td></tr>	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution\|Resolution]] 4.27Å</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=6k9l FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6k9l OCA], [~~http~~://pdbe.org/6k9l PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=6k9l RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/6k9l PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=6k9l ProSAT]</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=6k9l FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6k9l OCA], [https://pdbe.org/6k9l PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6k9l RCSB], [https://www.ebi.ac.uk/pdbsum/6k9l PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6k9l ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/ATM_HUMAN ATM_HUMAN]] Mantle cell lymphoma;B-cell chronic lymphocytic leukemia;Combined cervical dystonia;Ataxia-telangiectasia;Ataxia-telangiectasia variant. The disease is caused by mutations affecting the gene represented in this entry. Defects in ATM contribute to T-cell acute lymphoblastic leukemia (TALL) and T-prolymphocytic leukemia (TPLL). TPLL is characterized by a high white blood cell count, with a predominance of prolymphocytes, marked splenomegaly, lymphadenopathy, skin lesions and serous effusion. The clinical course is highly aggressive, with poor response to chemotherapy and short survival time. TPLL occurs both in adults as a sporadic disease and in younger AT patients.<ref>PMID:9288106</ref> <ref>PMID:9334731</ref> <ref>PMID:9463314</ref> <ref>PMID:9488043</ref> <ref>PMID:9573030</ref> Defects in ATM contribute to B-cell non-Hodgkin lymphomas (BNHL), including mantle cell lymphoma (MCL).<ref>PMID:10397742</ref> <ref>PMID:10706620</ref> <ref>PMID:9288106</ref> Defects in ATM contribute to B-cell chronic lymphocytic leukemia (BCLL). BCLL is the commonest form of leukemia in the elderly. It is characterized by the accumulation of mature CD5+ B-lymphocytes, lymphadenopathy, immunodeficiency and bone marrow failure.<ref>PMID:10023947</ref> <ref>PMID:10397742</ref> <ref>PMID:9892178</ref>	+	[https://www.uniprot.org/uniprot/ATM_HUMAN ATM_HUMAN] Mantle cell lymphoma;B-cell chronic lymphocytic leukemia;Combined cervical dystonia;Ataxia-telangiectasia;Ataxia-telangiectasia variant. The disease is caused by mutations affecting the gene represented in this entry. Defects in ATM contribute to T-cell acute lymphoblastic leukemia (TALL) and T-prolymphocytic leukemia (TPLL). TPLL is characterized by a high white blood cell count, with a predominance of prolymphocytes, marked splenomegaly, lymphadenopathy, skin lesions and serous effusion. The clinical course is highly aggressive, with poor response to chemotherapy and short survival time. TPLL occurs both in adults as a sporadic disease and in younger AT patients.<ref>PMID:9288106</ref> <ref>PMID:9334731</ref> <ref>PMID:9463314</ref> <ref>PMID:9488043</ref> <ref>PMID:9573030</ref> Defects in ATM contribute to B-cell non-Hodgkin lymphomas (BNHL), including mantle cell lymphoma (MCL).<ref>PMID:10397742</ref> <ref>PMID:10706620</ref> <ref>PMID:9288106</ref> Defects in ATM contribute to B-cell chronic lymphocytic leukemia (BCLL). BCLL is the commonest form of leukemia in the elderly. It is characterized by the accumulation of mature CD5+ B-lymphocytes, lymphadenopathy, immunodeficiency and bone marrow failure.<ref>PMID:10023947</ref> <ref>PMID:10397742</ref> <ref>PMID:9892178</ref>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/ATM_HUMAN ATM_HUMAN]] Serine/threonine protein kinase which activates checkpoint signaling upon double strand breaks (DSBs), apoptosis and genotoxic stresses such as ionizing ultraviolet A light (UVA), thereby acting as a DNA damage sensor. Recognizes the substrate consensus sequence [ST]-Q. Phosphorylates 'Ser-139' of histone variant H2AX/H2AFX at double strand breaks (DSBs), thereby regulating DNA damage response mechanism. Also plays a role in pre-B cell allelic exclusion, a process leading to expression of a single immunoglobulin heavy chain allele to enforce clonality and monospecific recognition by the B-cell antigen receptor (BCR) expressed on individual B-lymphocytes. After the introduction of DNA breaks by the RAG complex on one immunoglobulin allele, acts by mediating a repositioning of the second allele to pericentromeric heterochromatin, preventing accessibility to the RAG complex and recombination of the second allele. Also involved in signal transduction and cell cycle control. May function as a tumor suppressor. Necessary for activation of ABL1 and SAPK. Phosphorylates DYRK2, CHEK2, p53/TP53, FANCD2, NFKBIA, BRCA1, CTIP, nibrin (NBN), TERF1, RAD9 and DCLRE1C. May play a role in vesicle and/or protein transport. Could play a role in T-cell development, gonad and neurological function. Plays a role in replication-dependent histone mRNA degradation. Binds DNA ends. Phosphorylation of DYRK2 in nucleus in response to genotoxic stress prevents its MDM2-mediated ubiquitination and subsequent proteasome degradation. Phosphorylates ATF2 which stimulates its function in DNA damage response.<ref>PMID:10973490</ref> <ref>PMID:12556884</ref> <ref>PMID:14871926</ref> <ref>PMID:15916964</ref> <ref>PMID:16086026</ref> <ref>PMID:16858402</ref> <ref>PMID:17923702</ref> <ref>PMID:19965871</ref>	+	[https://www.uniprot.org/uniprot/ATM_HUMAN ATM_HUMAN] Serine/threonine protein kinase which activates checkpoint signaling upon double strand breaks (DSBs), apoptosis and genotoxic stresses such as ionizing ultraviolet A light (UVA), thereby acting as a DNA damage sensor. Recognizes the substrate consensus sequence [ST]-Q. Phosphorylates 'Ser-139' of histone variant H2AX/H2AFX at double strand breaks (DSBs), thereby regulating DNA damage response mechanism. Also plays a role in pre-B cell allelic exclusion, a process leading to expression of a single immunoglobulin heavy chain allele to enforce clonality and monospecific recognition by the B-cell antigen receptor (BCR) expressed on individual B-lymphocytes. After the introduction of DNA breaks by the RAG complex on one immunoglobulin allele, acts by mediating a repositioning of the second allele to pericentromeric heterochromatin, preventing accessibility to the RAG complex and recombination of the second allele. Also involved in signal transduction and cell cycle control. May function as a tumor suppressor. Necessary for activation of ABL1 and SAPK. Phosphorylates DYRK2, CHEK2, p53/TP53, FANCD2, NFKBIA, BRCA1, CTIP, nibrin (NBN), TERF1, RAD9 and DCLRE1C. May play a role in vesicle and/or protein transport. Could play a role in T-cell development, gonad and neurological function. Plays a role in replication-dependent histone mRNA degradation. Binds DNA ends. Phosphorylation of DYRK2 in nucleus in response to genotoxic stress prevents its MDM2-mediated ubiquitination and subsequent proteasome degradation. Phosphorylates ATF2 which stimulates its function in DNA damage response.<ref>PMID:10973490</ref> <ref>PMID:12556884</ref> <ref>PMID:14871926</ref> <ref>PMID:15916964</ref> <ref>PMID:16086026</ref> <ref>PMID:16858402</ref> <ref>PMID:17923702</ref> <ref>PMID:19965871</ref>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</SX>		</SX>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	~~[[Category: Non-specific serine/threonine protein kinase]]~~	+	[[Category: Chaban Y]]
-	[[Category: Chaban, Y]]	+	[[Category: Gao C]]
-	[[Category: Gao, C]]	+	[[Category: Li J]]
-	[[Category: Li, J]]	+	[[Category: Liu M]]
-	[[Category: Liu, M]]	+	[[Category: Qi Y]]
-	[[Category: Qi, Y]]	+	[[Category: Tian Y]]
-	[[Category: Tian, Y]]	+	[[Category: Xiao J]]
-	[[Category: Xiao, J]]	+	[[Category: Xu Y]]
-	[[Category: Xu, Y]]	+	[[Category: Yu Z]]
-	[[Category: Yu, Z]]	+	[[Category: Zhang P]]
-	[[Category: Zhang, P]]	+
-	~~[[Category: Cell cycle]]~~	+
-	~~[[Category: Dna damage response]]~~	+
-	~~[[Category: Kinase~~]]	+

OCA at 02:21, 11 April 2020

OCA — Sat, 11 Apr 2020 02:21:49 GMT

←Older revision		Revision as of 02:21, 11 April 2020
Line 3:		Line 3:
	<SX load='6k9l' size='340' side='right' viewer='molstar' caption='[[6k9l]], [[Resolution\|resolution]] 4.27Å' scene=''>		<SX load='6k9l' size='340' side='right' viewer='molstar' caption='[[6k9l]], [[Resolution\|resolution]] 4.27Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6k9l]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6K9L OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=6K9L FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6k9l]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6K9L OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=6K9L FirstGlance]. <br>
	</td></tr><tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Non-specific_serine/threonine_protein_kinase Non-specific serine/threonine protein kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.1 2.7.11.1] </span></td></tr>		</td></tr><tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Non-specific_serine/threonine_protein_kinase Non-specific serine/threonine protein kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.1 2.7.11.1] </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=6k9l FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6k9l OCA], [http://pdbe.org/6k9l PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6k9l RCSB], [http://www.ebi.ac.uk/pdbsum/6k9l PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6k9l 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=6k9l FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6k9l OCA], [http://pdbe.org/6k9l PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6k9l RCSB], [http://www.ebi.ac.uk/pdbsum/6k9l PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6k9l ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==

OCA at 22:23, 6 March 2020

OCA — Fri, 06 Mar 2020 22:23:29 GMT

←Older revision		Revision as of 22:23, 6 March 2020
Line 1:		Line 1:

	==4.27 Angstrom resolution cryo-EM structure of human dimeric ATM kinase==		==4.27 Angstrom resolution cryo-EM structure of human dimeric ATM kinase==
-	<~~StructureSection~~ load='6k9l' size='340' side='right'caption='[[6k9l]], [[Resolution\|resolution]] 4.27Å' scene=''>	+	<SX load='6k9l' size='340' side='right' viewer='molstar' caption='[[6k9l]], [[Resolution\|resolution]] 4.27Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[6k9l]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6K9L OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6K9L FirstGlance]. <br>		<table><tr><td colspan='2'>[[6k9l]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6K9L OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6K9L FirstGlance]. <br>
Line 14:		Line 14:
	<references/>		<references/>
	__TOC__		__TOC__
-	</~~StructureSection~~>	+	</SX>
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Non-specific serine/threonine protein kinase]]		[[Category: Non-specific serine/threonine protein kinase]]

OCA at 09:04, 25 December 2019

OCA — Wed, 25 Dec 2019 09:04:51 GMT

←Older revision		Revision as of 09:04, 25 December 2019
Line 1:		Line 1:
-	'''Unreleased structure'''

-	The entry ~~6k9l~~ is ~~ON HOLD~~ ~~until Paper Publication~~	+	==4.27 Angstrom resolution cryo-EM structure of human dimeric ATM kinase==
-		+	<StructureSection load='6k9l' size='340' side='right'caption='[[6k9l]], [[Resolution\|resolution]] 4.27Å' scene=''>
-	~~Authors~~:	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[6k9l]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6K9L OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6K9L FirstGlance]. <br>
-	~~Description:~~	+	</td></tr><tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Non-specific_serine/threonine_protein_kinase Non-specific serine/threonine protein kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.1 2.7.11.1] </span></td></tr>
-	[[Category: ~~Unreleased~~ Structures]]	+	<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=6k9l FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6k9l OCA], [http://pdbe.org/6k9l PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6k9l RCSB], [http://www.ebi.ac.uk/pdbsum/6k9l PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6k9l ProSAT]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/ATM_HUMAN ATM_HUMAN]] Mantle cell lymphoma;B-cell chronic lymphocytic leukemia;Combined cervical dystonia;Ataxia-telangiectasia;Ataxia-telangiectasia variant. The disease is caused by mutations affecting the gene represented in this entry. Defects in ATM contribute to T-cell acute lymphoblastic leukemia (TALL) and T-prolymphocytic leukemia (TPLL). TPLL is characterized by a high white blood cell count, with a predominance of prolymphocytes, marked splenomegaly, lymphadenopathy, skin lesions and serous effusion. The clinical course is highly aggressive, with poor response to chemotherapy and short survival time. TPLL occurs both in adults as a sporadic disease and in younger AT patients.<ref>PMID:9288106</ref> <ref>PMID:9334731</ref> <ref>PMID:9463314</ref> <ref>PMID:9488043</ref> <ref>PMID:9573030</ref> Defects in ATM contribute to B-cell non-Hodgkin lymphomas (BNHL), including mantle cell lymphoma (MCL).<ref>PMID:10397742</ref> <ref>PMID:10706620</ref> <ref>PMID:9288106</ref> Defects in ATM contribute to B-cell chronic lymphocytic leukemia (BCLL). BCLL is the commonest form of leukemia in the elderly. It is characterized by the accumulation of mature CD5+ B-lymphocytes, lymphadenopathy, immunodeficiency and bone marrow failure.<ref>PMID:10023947</ref> <ref>PMID:10397742</ref> <ref>PMID:9892178</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/ATM_HUMAN ATM_HUMAN]] Serine/threonine protein kinase which activates checkpoint signaling upon double strand breaks (DSBs), apoptosis and genotoxic stresses such as ionizing ultraviolet A light (UVA), thereby acting as a DNA damage sensor. Recognizes the substrate consensus sequence [ST]-Q. Phosphorylates 'Ser-139' of histone variant H2AX/H2AFX at double strand breaks (DSBs), thereby regulating DNA damage response mechanism. Also plays a role in pre-B cell allelic exclusion, a process leading to expression of a single immunoglobulin heavy chain allele to enforce clonality and monospecific recognition by the B-cell antigen receptor (BCR) expressed on individual B-lymphocytes. After the introduction of DNA breaks by the RAG complex on one immunoglobulin allele, acts by mediating a repositioning of the second allele to pericentromeric heterochromatin, preventing accessibility to the RAG complex and recombination of the second allele. Also involved in signal transduction and cell cycle control. May function as a tumor suppressor. Necessary for activation of ABL1 and SAPK. Phosphorylates DYRK2, CHEK2, p53/TP53, FANCD2, NFKBIA, BRCA1, CTIP, nibrin (NBN), TERF1, RAD9 and DCLRE1C. May play a role in vesicle and/or protein transport. Could play a role in T-cell development, gonad and neurological function. Plays a role in replication-dependent histone mRNA degradation. Binds DNA ends. Phosphorylation of DYRK2 in nucleus in response to genotoxic stress prevents its MDM2-mediated ubiquitination and subsequent proteasome degradation. Phosphorylates ATF2 which stimulates its function in DNA damage response.<ref>PMID:10973490</ref> <ref>PMID:12556884</ref> <ref>PMID:14871926</ref> <ref>PMID:15916964</ref> <ref>PMID:16086026</ref> <ref>PMID:16858402</ref> <ref>PMID:17923702</ref> <ref>PMID:19965871</ref>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Large Structures]]
		+	[[Category: Non-specific serine/threonine protein kinase]]
		+	[[Category: Chaban, Y]]
		+	[[Category: Gao, C]]
		+	[[Category: Li, J]]
		+	[[Category: Liu, M]]
		+	[[Category: Qi, Y]]
		+	[[Category: Tian, Y]]
		+	[[Category: Xiao, J]]
		+	[[Category: Xu, Y]]
		+	[[Category: Yu, Z]]
		+	[[Category: Zhang, P]]
		+	[[Category: Cell cycle]]
		+	[[Category: Dna damage response]]
		+	[[Category: Kinase]]

OCA at 09:13, 13 November 2019

OCA — Wed, 13 Nov 2019 09:13:18 GMT

←Older revision		Revision as of 09:13, 13 November 2019
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 6k9l is ON HOLD	+	The entry 6k9l is ON HOLD until Paper Publication

	Authors:		Authors:

OCA: Protected "6k9l" [edit=sysop:move=sysop]

OCA — Wed, 26 Jun 2019 05:05:55 GMT

Protected "6k9l" [edit=sysop:move=sysop]

←Older revision

Revision as of 05:05, 26 June 2019

OCA: New page: '''Unreleased structure''' The entry 6k9l is ON HOLD Authors: Description: Category: Unreleased Structures

OCA — Wed, 26 Jun 2019 05:05:54 GMT

New page: '''Unreleased structure''' The entry 6k9l is ON HOLD Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 6k9l is ON HOLD

Authors:

Description:
[[Category: Unreleased Structures]]