5hye - Revision history

OCA at 11:00, 16 August 2023

OCA — Wed, 16 Aug 2023 11:00:19 GMT

←Older revision		Revision as of 11:00, 16 August 2023
Line 1:		Line 1:

	==Glycosylated Knob-Knob Fc fragment (P212121)==		==Glycosylated Knob-Knob Fc fragment (P212121)==
-	<StructureSection load='5hye' size='340' side='right' caption='[[5hye]], [[Resolution\|resolution]] 1.89Å' scene=''>	+	<StructureSection load='5hye' size='340' side='right'caption='[[5hye]], [[Resolution\|resolution]] 1.89Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5hye]] is a 2 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/~~Human Human~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5HYE OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5HYE FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5hye]] 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=5HYE OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5HYE FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=BMA:BETA-D-MANNOSE'>BMA</scene>, <scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=GAL:BETA-D-GALACTOSE'>GAL</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</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]] 1.89Å</td></tr>
-	~~<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5hy9\|5hy9]]</td></tr>~~	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=BMA:BETA-D-MANNOSE'>BMA</scene>, <scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=GAL:BETA-D-GALACTOSE'>GAL</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
-	~~<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">IGHG1 ([http://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=5hye FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5hye OCA], [https://pdbe.org/5hye PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5hye RCSB], [https://www.ebi.ac.uk/pdbsum/5hye PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5hye ProSAT]</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=5hye FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5hye OCA], [~~http~~://pdbe.org/5hye PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=5hye RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/5hye PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=5hye ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/IGHG1_HUMAN IGHG1_HUMAN]] Defects in IGHG1 are a cause of multiple myeloma (MM) [MIM:[~~http~~://omim.org/entry/254500 254500]]. MM is a malignant tumor of plasma cells usually arising in the bone marrow and characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria and anemia. Complications of multiple myeloma are bone pain, hypercalcemia, renal failure and spinal cord compression. The aberrant antibodies that are produced lead to impaired humoral immunity and patients have a high prevalence of infection. Amyloidosis may develop in some patients. Multiple myeloma is part of a spectrum of diseases ranging from monoclonal gammopathy of unknown significance (MGUS) to plasma cell leukemia. Note=A chromosomal aberration involving IGHG1 is found in multiple myeloma. Translocation t(11;14)(q13;q32) with the IgH locus. Translocation t(11;14)(q13;q32) with CCND1; translocation t(4;14)(p16.3;q32.3) with FGFR3; translocation t(6;14)(p25;q32) with IRF4.	+	[https://www.uniprot.org/uniprot/IGHG1_HUMAN IGHG1_HUMAN] Defects in IGHG1 are a cause of multiple myeloma (MM) [MIM:[https://omim.org/entry/254500 254500]. MM is a malignant tumor of plasma cells usually arising in the bone marrow and characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria and anemia. Complications of multiple myeloma are bone pain, hypercalcemia, renal failure and spinal cord compression. The aberrant antibodies that are produced lead to impaired humoral immunity and patients have a high prevalence of infection. Amyloidosis may develop in some patients. Multiple myeloma is part of a spectrum of diseases ranging from monoclonal gammopathy of unknown significance (MGUS) to plasma cell leukemia. Note=A chromosomal aberration involving IGHG1 is found in multiple myeloma. Translocation t(11;14)(q13;q32) with the IgH locus. Translocation t(11;14)(q13;q32) with CCND1; translocation t(4;14)(p16.3;q32.3) with FGFR3; translocation t(6;14)(p25;q32) with IRF4.
		+	== Function ==
		+	[https://www.uniprot.org/uniprot/IGHG1_HUMAN IGHG1_HUMAN]
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 24:		Line 25:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
-	[[Category: ~~Benz, J~~]]	+	[[Category: Large Structures]]
-	[[Category: ~~Kuglstatter, A~~]]	+	[[Category: Benz J]]
-	[[Category: ~~Stihle, M~~]]	+	[[Category: Kuglstatter A]]
-	[[Category: ~~Bispecific antibody fc engineering knob-into-hole]]~~	+	[[Category: Stihle M]]
-	~~[[Category: Immune system~~]]	+

OCA at 07:35, 6 December 2017

OCA — Wed, 06 Dec 2017 07:35:44 GMT

←Older revision		Revision as of 07:35, 6 December 2017
Line 3:		Line 3:
	<StructureSection load='5hye' size='340' side='right' caption='[[5hye]], [[Resolution\|resolution]] 1.89Å' scene=''>		<StructureSection load='5hye' size='340' side='right' caption='[[5hye]], [[Resolution\|resolution]] 1.89Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5hye]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5HYE OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5HYE FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5hye]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5HYE OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5HYE FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=BMA:BETA-D-MANNOSE'>BMA</scene>, <scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=GAL:BETA-D-GALACTOSE'>GAL</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=BMA:BETA-D-MANNOSE'>BMA</scene>, <scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=GAL:BETA-D-GALACTOSE'>GAL</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5hy9\|5hy9]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5hy9\|5hy9]]</td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">IGHG1 ([http://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'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5hye FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5hye OCA], [http://pdbe.org/5hye PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5hye RCSB], [http://www.ebi.ac.uk/pdbsum/5hye PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5hye ProSAT]</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=5hye FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5hye OCA], [http://pdbe.org/5hye PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5hye RCSB], [http://www.ebi.ac.uk/pdbsum/5hye PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5hye ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/IGHG1_HUMAN IGHG1_HUMAN]] Defects in IGHG1 are a cause of multiple myeloma (MM) [MIM:[http://omim.org/entry/254500 254500]]. MM is a malignant tumor of plasma cells usually arising in the bone marrow and characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria and anemia. Complications of multiple myeloma are bone pain, hypercalcemia, renal failure and spinal cord compression. The aberrant antibodies that are produced lead to impaired humoral immunity and patients have a high prevalence of infection. Amyloidosis may develop in some patients. Multiple myeloma is part of a spectrum of diseases ranging from monoclonal gammopathy of unknown significance (MGUS) to plasma cell leukemia. Note=A chromosomal aberration involving IGHG1 is found in multiple myeloma. Translocation t(11;14)(q13;q32) with the IgH locus. Translocation t(11;14)(q13;q32) with CCND1; translocation t(4;14)(p16.3;q32.3) with FGFR3; translocation t(6;14)(p25;q32) with IRF4.		[[http://www.uniprot.org/uniprot/IGHG1_HUMAN IGHG1_HUMAN]] Defects in IGHG1 are a cause of multiple myeloma (MM) [MIM:[http://omim.org/entry/254500 254500]]. MM is a malignant tumor of plasma cells usually arising in the bone marrow and characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria and anemia. Complications of multiple myeloma are bone pain, hypercalcemia, renal failure and spinal cord compression. The aberrant antibodies that are produced lead to impaired humoral immunity and patients have a high prevalence of infection. Amyloidosis may develop in some patients. Multiple myeloma is part of a spectrum of diseases ranging from monoclonal gammopathy of unknown significance (MGUS) to plasma cell leukemia. Note=A chromosomal aberration involving IGHG1 is found in multiple myeloma. Translocation t(11;14)(q13;q32) with the IgH locus. Translocation t(11;14)(q13;q32) with CCND1; translocation t(4;14)(p16.3;q32.3) with FGFR3; translocation t(6;14)(p25;q32) with IRF4.
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	An increasing number of bispecific therapeutic antibodies are progressing through clinical development. The Knob-into-Hole (KiH) technology uses complementary mutations in the CH3 region of the antibody Fc fragment to achieve heavy chain heterodimerization. Here we describe the X-ray crystal structures of glycosylated and disulfide-engineered heterodimeric KiH Fc fragment and its homodimeric Knob-Knob and Hole-Hole side products. The heterodimer structure confirms the KiH design principle and supports the hypothesis that glycosylation stabilizes a closed Fc conformation. Both homodimer structures show parallel Fc fragment architectures, in contrast to recently reported crystal structures of the corresponding aglycosylated Fc fragments which in the absence of disulfide mutations show an unexpected antiparallel arrangement. The glycosylated Knob-Knob Fc fragment is destabilized as indicated by variability in the relative orientation of its CH3 domains. The glycosylated Hole-Hole Fc fragment shows an unexpected intermolecular disulfide bond via the introduced Y349C Hole mutation which results in a large CH3 domain shift and a new CH3-CH3 interface. The crystal structures of glycosylated, disulfide-linked KiH Fc fragment and its Knob-Knob and Hole-Hole side products reported here will facilitate further design of highly efficient antibody heterodimerization strategies.
		+
		+	Structural differences between glycosylated, disulfide-linked heterodimeric Knob-into-Hole Fc fragment and its homodimeric Knob-Knob and Hole-Hole side products.,Kuglstatter A, Stihle M, Neumann C, Muller C, Schaefer W, Klein C, Benz J Protein Eng Des Sel. 2017 Sep 1;30(9):649-656. doi: 10.1093/protein/gzx041. PMID:28985438<ref>PMID:28985438</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 5hye" style="background-color:#fffaf0;"></div>
		+	== References ==
		+	<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Human]]
	[[Category: Benz, J]]		[[Category: Benz, J]]
	[[Category: Kuglstatter, A]]		[[Category: Kuglstatter, A]]

OCA at 18:06, 1 February 2017

OCA — Wed, 01 Feb 2017 18:06:34 GMT

←Older revision		Revision as of 18:06, 1 February 2017
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 5hye is ~~ON HOLD until Paper Publication~~	+	==Glycosylated Knob-Knob Fc fragment (P212121)==
-		+	<StructureSection load='5hye' size='340' side='right' caption='[[5hye]], [[Resolution\|resolution]] 1.89Å' scene=''>
-	~~Authors~~:	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[5hye]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5HYE OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5HYE FirstGlance]. <br>
-	~~Description~~:	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=BMA:BETA-D-MANNOSE'>BMA</scene>, <scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=GAL:BETA-D-GALACTOSE'>GAL</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
-	[[Category: ~~Unreleased Structures~~]]	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5hy9\|5hy9]]</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=5hye FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5hye OCA], [http://pdbe.org/5hye PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5hye RCSB], [http://www.ebi.ac.uk/pdbsum/5hye PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5hye ProSAT]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/IGHG1_HUMAN IGHG1_HUMAN]] Defects in IGHG1 are a cause of multiple myeloma (MM) [MIM:[http://omim.org/entry/254500 254500]]. MM is a malignant tumor of plasma cells usually arising in the bone marrow and characterized by diffuse involvement of the skeletal system, hyperglobulinemia, Bence-Jones proteinuria and anemia. Complications of multiple myeloma are bone pain, hypercalcemia, renal failure and spinal cord compression. The aberrant antibodies that are produced lead to impaired humoral immunity and patients have a high prevalence of infection. Amyloidosis may develop in some patients. Multiple myeloma is part of a spectrum of diseases ranging from monoclonal gammopathy of unknown significance (MGUS) to plasma cell leukemia. Note=A chromosomal aberration involving IGHG1 is found in multiple myeloma. Translocation t(11;14)(q13;q32) with the IgH locus. Translocation t(11;14)(q13;q32) with CCND1; translocation t(4;14)(p16.3;q32.3) with FGFR3; translocation t(6;14)(p25;q32) with IRF4.
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Benz, J]]
		+	[[Category: Kuglstatter, A]]
		+	[[Category: Stihle, M]]
		+	[[Category: Bispecific antibody fc engineering knob-into-hole]]
		+	[[Category: Immune system]]

OCA at 14:00, 15 May 2016

OCA — Sun, 15 May 2016 14:00:21 GMT

←Older revision		Revision as of 14:00, 15 May 2016
Line 3:		Line 3:
	The entry 5hye is ON HOLD until Paper Publication		The entry 5hye is ON HOLD until Paper Publication

-	Authors: ~~Kuglstatter, A., Stihle, M., Benz, J.~~	+	Authors:

	Description:		Description:
	[[Category: Unreleased Structures]]		[[Category: Unreleased Structures]]
-	[[Category: Kuglstatter, A]]
-	[[Category: Benz, J]]
-	[[Category: Stihle, M]]

OCA at 00:02, 11 May 2016

OCA — Wed, 11 May 2016 00:02:45 GMT

←Older revision		Revision as of 00:02, 11 May 2016
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 5hye is ON HOLD	+	The entry 5hye is ON HOLD until Paper Publication

	Authors: Kuglstatter, A., Stihle, M., Benz, J.		Authors: Kuglstatter, A., Stihle, M., Benz, J.

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

OCA — Wed, 10 Feb 2016 15:53:56 GMT

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

←Older revision

Revision as of 15:53, 10 February 2016

OCA: New page: '''Unreleased structure''' The entry 5hye is ON HOLD Authors: Kuglstatter, A., Stihle, M., Benz, J. Description: Category: Unreleased Structures Category: Kuglstatter, A [[Cat...

OCA — Wed, 10 Feb 2016 15:53:54 GMT

New page: '''Unreleased structure''' The entry 5hye is ON HOLD Authors: Kuglstatter, A., Stihle, M., Benz, J. Description: Category: Unreleased Structures Category: Kuglstatter, A [[Cat...

New page

'''Unreleased structure'''

The entry 5hye is ON HOLD

Authors: Kuglstatter, A., Stihle, M., Benz, J.

Description:
[[Category: Unreleased Structures]]
[[Category: Kuglstatter, A]]
[[Category: Benz, J]]
[[Category: Stihle, M]]