6g1l - Revision history

OCA at 10:24, 18 March 2021

2021-03-18T10:24:02Z

←Older revision		Revision as of 10:24, 18 March 2021
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	==MITF/CLEARbox structure==		==MITF/CLEARbox structure==
-	<StructureSection load='6g1l' size='340' side='right' caption='[[6g1l]], [[Resolution\|resolution]] 2.40Å' scene=''>	+	<StructureSection load='6g1l' size='340' side='right'caption='[[6g1l]], [[Resolution\|resolution]] 2.40Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[6g1l]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6G1L OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=6G1L FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[6g1l]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6G1L OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6G1L FirstGlance]. <br>
-	</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=6g1l FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6g1l OCA], [~~http~~://pdbe.org/6g1l PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=6g1l RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/6g1l PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=6g1l ProSAT]</span></td></tr>	+	</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=6g1l FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6g1l OCA], [https://pdbe.org/6g1l PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6g1l RCSB], [https://www.ebi.ac.uk/pdbsum/6g1l PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6g1l ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/MITF_MOUSE MITF_MOUSE]] Defects in Mitf are the cause of microphthalmia (mi), a condition characterized by loss of pigmentation; reduced eye size; failure of secondary bone resorption; reduced numbers of mast cells; early onset of deafness, and which gives rise to a number of different phenotypes. Among them, microphthalmia-eyeless white (mi-ew) has a normal appearance at the heterozygous state, but shows white coat; eyes almost absent and eyelids never open at homozygosity. Microphthalmia-black and white spot (mi-bws) is normal at heterozygosity, and presents white spots and black eyes at homozygous state. Microphthalmia-white (mi-wh) has reduced coat color and eye pigmentation; spots on toes, tail and belly; inner ear defects at heterozygosity, and at homozygosity shows white coat; eyes small and inner iris slightly pigmented; spinal ganglia, adrenal medulla and dermis smaller than normal, and inner ear defects. Microphthalmia-vitiligo (mi-vi) has normal phenotype at heterozygosity, but shows gradual depigmentation of coat, skin and eyes; and retinal degeneration at homozygosity. Microphthalmia-spotted (mi-sp) shows normal phenotype; at homozygosity, however, tyrosinase activity in skin is reduced. Microphthalmia-defective irism (mi-di) has reduced retinal pigmentation at heterozygosity and shows white coat; eyes of reduced sized and possible mild osteoporosis at homozygosity. Microphthalmia-cloudy eyed (mi-ce) has a normal appearance at the heterozygous state, but shows white coat; eyes of reduced size and unpigmented at homozygosity. Microphthalmia-red-eyed white (mi-rw) has a normal appearance at the homozygous state, but shows white coat with one or more pigmented spots around the head/and or tail; eyes are small and red at heterozygosity. Microphthalmia-black-eyed white (mi-bw) shows a white coat but normal sized eyes which reamin black at homozygosity.	+	[[https://www.uniprot.org/uniprot/MITF_MOUSE MITF_MOUSE]] Defects in Mitf are the cause of microphthalmia (mi), a condition characterized by loss of pigmentation; reduced eye size; failure of secondary bone resorption; reduced numbers of mast cells; early onset of deafness, and which gives rise to a number of different phenotypes. Among them, microphthalmia-eyeless white (mi-ew) has a normal appearance at the heterozygous state, but shows white coat; eyes almost absent and eyelids never open at homozygosity. Microphthalmia-black and white spot (mi-bws) is normal at heterozygosity, and presents white spots and black eyes at homozygous state. Microphthalmia-white (mi-wh) has reduced coat color and eye pigmentation; spots on toes, tail and belly; inner ear defects at heterozygosity, and at homozygosity shows white coat; eyes small and inner iris slightly pigmented; spinal ganglia, adrenal medulla and dermis smaller than normal, and inner ear defects. Microphthalmia-vitiligo (mi-vi) has normal phenotype at heterozygosity, but shows gradual depigmentation of coat, skin and eyes; and retinal degeneration at homozygosity. Microphthalmia-spotted (mi-sp) shows normal phenotype; at homozygosity, however, tyrosinase activity in skin is reduced. Microphthalmia-defective irism (mi-di) has reduced retinal pigmentation at heterozygosity and shows white coat; eyes of reduced sized and possible mild osteoporosis at homozygosity. Microphthalmia-cloudy eyed (mi-ce) has a normal appearance at the heterozygous state, but shows white coat; eyes of reduced size and unpigmented at homozygosity. Microphthalmia-red-eyed white (mi-rw) has a normal appearance at the homozygous state, but shows white coat with one or more pigmented spots around the head/and or tail; eyes are small and red at heterozygosity. Microphthalmia-black-eyed white (mi-bw) shows a white coat but normal sized eyes which reamin black at homozygosity.
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/MITF_MOUSE MITF_MOUSE]] Transcription factor that regulates the expression of genes with essential roles in cell differentiation, proliferation and survival. Binds to symmetrical DNA sequences (E-boxes) (5'-CACGTG-3') found in the promoters of target genes, such as BCL2 and tyrosinase (TYR). Plays an important role in melanocyte development by regulating the expression of tyrosinase (TYR) and tyrosinase-related protein 1 (TYRP1). Plays a critical role in the differentiation of various cell types, such as neural crest-derived melanocytes, mast cells, osteoclasts and optic cup-derived retinal pigment epithelium.	+	[[https://www.uniprot.org/uniprot/MITF_MOUSE MITF_MOUSE]] Transcription factor that regulates the expression of genes with essential roles in cell differentiation, proliferation and survival. Binds to symmetrical DNA sequences (E-boxes) (5'-CACGTG-3') found in the promoters of target genes, such as BCL2 and tyrosinase (TYR). Plays an important role in melanocyte development by regulating the expression of tyrosinase (TYR) and tyrosinase-related protein 1 (TYRP1). Plays a critical role in the differentiation of various cell types, such as neural crest-derived melanocytes, mast cells, osteoclasts and optic cup-derived retinal pigment epithelium.
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
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	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Large Structures]]
	[[Category: Pogenberg, V]]		[[Category: Pogenberg, V]]
	[[Category: Wilmanns, M]]		[[Category: Wilmanns, M]]

OCA at 09:48, 13 February 2019

2019-02-13T09:48:40Z

←Older revision		Revision as of 09:48, 13 February 2019
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-	'''Unreleased structure'''

-	~~The entry~~ 6g1l is ~~ON HOLD until Paper~~ Publication	+	==MITF/CLEARbox structure==
		+	<StructureSection load='6g1l' size='340' side='right' caption='[[6g1l]], [[Resolution\|resolution]] 2.40Å' scene=''>
		+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[6g1l]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6G1L OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6G1L FirstGlance]. <br>
		+	</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=6g1l FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6g1l OCA], [http://pdbe.org/6g1l PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6g1l RCSB], [http://www.ebi.ac.uk/pdbsum/6g1l PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6g1l ProSAT]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/MITF_MOUSE MITF_MOUSE]] Defects in Mitf are the cause of microphthalmia (mi), a condition characterized by loss of pigmentation; reduced eye size; failure of secondary bone resorption; reduced numbers of mast cells; early onset of deafness, and which gives rise to a number of different phenotypes. Among them, microphthalmia-eyeless white (mi-ew) has a normal appearance at the heterozygous state, but shows white coat; eyes almost absent and eyelids never open at homozygosity. Microphthalmia-black and white spot (mi-bws) is normal at heterozygosity, and presents white spots and black eyes at homozygous state. Microphthalmia-white (mi-wh) has reduced coat color and eye pigmentation; spots on toes, tail and belly; inner ear defects at heterozygosity, and at homozygosity shows white coat; eyes small and inner iris slightly pigmented; spinal ganglia, adrenal medulla and dermis smaller than normal, and inner ear defects. Microphthalmia-vitiligo (mi-vi) has normal phenotype at heterozygosity, but shows gradual depigmentation of coat, skin and eyes; and retinal degeneration at homozygosity. Microphthalmia-spotted (mi-sp) shows normal phenotype; at homozygosity, however, tyrosinase activity in skin is reduced. Microphthalmia-defective irism (mi-di) has reduced retinal pigmentation at heterozygosity and shows white coat; eyes of reduced sized and possible mild osteoporosis at homozygosity. Microphthalmia-cloudy eyed (mi-ce) has a normal appearance at the heterozygous state, but shows white coat; eyes of reduced size and unpigmented at homozygosity. Microphthalmia-red-eyed white (mi-rw) has a normal appearance at the homozygous state, but shows white coat with one or more pigmented spots around the head/and or tail; eyes are small and red at heterozygosity. Microphthalmia-black-eyed white (mi-bw) shows a white coat but normal sized eyes which reamin black at homozygosity.
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/MITF_MOUSE MITF_MOUSE]] Transcription factor that regulates the expression of genes with essential roles in cell differentiation, proliferation and survival. Binds to symmetrical DNA sequences (E-boxes) (5'-CACGTG-3') found in the promoters of target genes, such as BCL2 and tyrosinase (TYR). Plays an important role in melanocyte development by regulating the expression of tyrosinase (TYR) and tyrosinase-related protein 1 (TYRP1). Plays a critical role in the differentiation of various cell types, such as neural crest-derived melanocytes, mast cells, osteoclasts and optic cup-derived retinal pigment epithelium.
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	The MITF transcription factor is a master regulator of melanocyte development and a critical factor in melanomagenesis. The related transcription factors TFEB and TFE3 regulate lysosomal activity and autophagy processes known to be important in melanoma. Here we show that MITF binds the CLEAR-box element in the promoters of lysosomal and autophagosomal genes in melanocytes and melanoma cells. The crystal structure of MITF bound to the CLEAR-box reveals how the palindromic nature of this motif induces symmetric MITF homodimer binding. In metastatic melanoma tumors and cell lines, MITF positively correlates with the expression of lysosomal and autophagosomal genes, which, interestingly, are different from the lysosomal and autophagosomal genes correlated with TFEB and TFE3. Depletion of MITF in melanoma cells and melanocytes attenuates the response to starvation-induced autophagy, whereas the overexpression of MITF in melanoma cells increases the number of autophagosomes but is not sufficient to induce autophagic flux. Our results suggest that MITF and the related factors TFEB and TFE3 have separate roles in regulating a starvation-induced autophagy response in melanoma. Understanding the normal and pathophysiological roles of MITF and related transcription factors may provide important clinical insights into melanoma therapy.

-	~~Authors:~~ Pogenberg, V., ~~Wilmanns~~, M.	+	MITF has a central role in regulating starvation-induced autophagy in melanoma.,Moller K, Sigurbjornsdottir S, Arnthorsson AO, Pogenberg V, Dilshat R, Fock V, Brynjolfsdottir SH, Bindesboll C, Bessadottir M, Ogmundsdottir HM, Simonsen A, Larue L, Wilmanns M, Thorsson V, Steingrimsson E, Ogmundsdottir MH Sci Rep. 2019 Jan 31;9(1):1055. doi: 10.1038/s41598-018-37522-6. PMID:30705290<ref>PMID:30705290</ref>

-	~~Description: MITF~~/~~CLEARbox structure~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[Category~~: ~~Unreleased Structures]]~~	+	</div>
		+	<div class="pdbe-citations 6g1l" style="background-color:#fffaf0;"></div>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
	[[Category: Pogenberg, V]]		[[Category: Pogenberg, V]]
	[[Category: Wilmanns, M]]		[[Category: Wilmanns, M]]
		+	[[Category: Autophagy]]
		+	[[Category: Dna binding]]
		+	[[Category: Melanocyte]]
		+	[[Category: Transcription]]
		+	[[Category: Transcription factor]]

OCA at 04:47, 4 April 2018

2018-04-04T04:47:14Z

←Older revision		Revision as of 04:47, 4 April 2018
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	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 6g1l is ON HOLD	+	The entry 6g1l is ON HOLD until Paper Publication

	Authors: Pogenberg, V., Wilmanns, M.		Authors: Pogenberg, V., Wilmanns, M.
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	Description: MITF/CLEARbox structure		Description: MITF/CLEARbox structure
	[[Category: Unreleased Structures]]		[[Category: Unreleased Structures]]
-	[[Category: Wilmanns, M]]
	[[Category: Pogenberg, V]]		[[Category: Pogenberg, V]]
		+	[[Category: Wilmanns, M]]

OCA: Protected "6g1l" [edit=sysop:move=sysop]

2018-03-28T05:30:23Z

Protected "6g1l" [edit=sysop:move=sysop]

←Older revision

Revision as of 05:30, 28 March 2018

OCA: New page: '''Unreleased structure''' The entry 6g1l is ON HOLD Authors: Pogenberg, V., Wilmanns, M. Description: MITF/CLEARbox structure Category: Unreleased Structures [[Category: Wilmanns,...

2018-03-28T05:30:22Z

New page: '''Unreleased structure''' The entry 6g1l is ON HOLD Authors: Pogenberg, V., Wilmanns, M. Description: MITF/CLEARbox structure Category: Unreleased Structures [[Category: Wilmanns,...

New page

'''Unreleased structure'''

The entry 6g1l is ON HOLD

Authors: Pogenberg, V., Wilmanns, M.

Description: MITF/CLEARbox structure
[[Category: Unreleased Structures]]
[[Category: Wilmanns, M]]
[[Category: Pogenberg, V]]