Developmental Signals - Sox - Revision history

Z8600021 at 23:01, 26 March 2020

2020-03-26T23:01:01Z

← Older revision		Revision as of 09:01, 27 March 2020
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	\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}		\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}

	Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Sox+Expression ''Sox Expression'']		Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Sox+Expression ''Sox Expression''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Morula+Sox2 ''Morula+Sox2''] \| [http://www.ncbi.nlm.nih.gov/pubmed/?term=Blastcyst+Sox2 ''Blastcyst+Sox2'']
	\|}		\|}
	{\| class="wikitable mw-collapsible mw-collapsed"		{\| class="wikitable mw-collapsible mw-collapsed"
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	===SOX2===		===SOX2===

			In the {{mouse}} {{blastocyst}} Sox2 forms a complex with Oct4 to maintain self-renewal of the pluripotent inner cell mass (ICM) and is also required for the formation of {{trophectoderm}}.{{#pmid:21103067\|PMID21103067}}

	{\|		{\|
	\|		\|
	* Sox2 is first expressed in very early (morula, blastocyst) development.		* Sox2 is first expressed in very early ({{morula}}, {{blastocyst}}) development.
	* Forms a trimeric transcription complex with OCT4.		* Forms a trimeric transcription complex with OCT4.
	* Gene targets - YES1, FGF4, UTF1 and ZFP206.		* Gene targets - YES1, FGF4, UTF1 and ZFP206.

Z8600021 at 00:21, 7 November 2019

2019-11-07T00:21:57Z

← Older revision		Revision as of 10:21, 7 November 2019
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	* '''Distinct SoxB1 networks are required for naïve and primed pluripotency'''{{#pmid:29256862\|PMID29256862}} "Deletion of Sox2 from mouse embryonic stem cells (ESCs) causes trophectodermal differentiation. While this can be prevented by enforced expression of the related SOXB1 proteins, SOX1 or SOX3, the roles of SOXB1 proteins in epiblast stem cell (EpiSC) pluripotency are unknown. Here, we show that Sox2 can be deleted from EpiSCs with impunity. This is due to a shift in the balance of SoxB1 expression in EpiSCs, which have decreased Sox2 and increased Sox3 compared to ESCs. Consistent with functional redundancy, Sox3 can also be deleted from EpiSCs without eliminating self-renewal. However, deletion of both Sox2 and Sox3 prevents self-renewal. The overall SOXB1 levels in ESCs affect differentiation choices: neural differentiation of Sox2 heterozygous ESCs is compromised, while increased SOXB1 levels divert the ESC to EpiSC transition towards neural differentiation. Therefore, optimal SOXB1 levels are critical for each pluripotent state and for cell fate decisions during exit from naïve pluripotency." [[Stem Cells]]		* '''Distinct SoxB1 networks are required for naïve and primed pluripotency'''{{#pmid:29256862\|PMID29256862}} "Deletion of Sox2 from mouse embryonic stem cells (ESCs) causes trophectodermal differentiation. While this can be prevented by enforced expression of the related SOXB1 proteins, SOX1 or SOX3, the roles of SOXB1 proteins in epiblast stem cell (EpiSC) pluripotency are unknown. Here, we show that Sox2 can be deleted from EpiSCs with impunity. This is due to a shift in the balance of SoxB1 expression in EpiSCs, which have decreased Sox2 and increased Sox3 compared to ESCs. Consistent with functional redundancy, Sox3 can also be deleted from EpiSCs without eliminating self-renewal. However, deletion of both Sox2 and Sox3 prevents self-renewal. The overall SOXB1 levels in ESCs affect differentiation choices: neural differentiation of Sox2 heterozygous ESCs is compromised, while increased SOXB1 levels divert the ESC to EpiSC transition towards neural differentiation. Therefore, optimal SOXB1 levels are critical for each pluripotent state and for cell fate decisions during exit from naïve pluripotency." [[Stem Cells]]

	* '''Long-term expandable SOX9+ chondrogenic ectomesenchymal cells from human pluripotent stem cells'''{{#pmid:25818812\|PMID25818812}} "Here we report the successful generation and long-term expansion of SOX9-expressing CD271(+)PDGFRα(+)CD73(+) chondrogenic ectomesenchymal cells from the PAX3/SOX10/FOXD3-expressing MIXL1(-)CD271(hi)PDGFRα(lo)CD73(-) neural crest-like progeny of human pluripotent stem cells in a chemically defined medium supplemented with Nodal/Activin/transforming growth factorβ (TGFβ) inhibitor and fibroblast growth factor (FGF). When "primed" with TGFβ, such cells efficiently formed translucent cartilage particles, which were completely mineralized in 12 weeks in immunocompromized mice." [[Musculoskeletal System - Cartilage Development\|Cartilage Development]]
	* '''Just how conserved is vertebrate sex determination?'''<ref name="PMID23390004"><pubmed>23390004</pubmed></ref> "Sex determination in vertebrate embryos has long been equated with gonadal differentiation into testes or ovaries. This view has been challenged over the years by reports of somatic sexual dimorphisms pre-dating gonadal sex differentiation. ...We illustrate these differences by comparing key sex genes in fishes versus birds and mammals, with emphasis on DM domain genes, the SOX-9AMH pathway in the testis and the FOXL2-Aromatase pathway in the ovary. Such comparisons facilitate the identification of ancient versus derived genes involved in gonadal sex determination. The data indicate that vertebrate sex-determining cascades are not as conserved as once thought."

	\|}		\|}
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	\|-		\|-
	\| {{Older papers}}		\| {{Older papers}}
			* '''Long-term expandable SOX9+ chondrogenic ectomesenchymal cells from human pluripotent stem cells'''{{#pmid:25818812\|PMID25818812}} "Here we report the successful generation and long-term expansion of SOX9-expressing CD271(+)PDGFRα(+)CD73(+) chondrogenic ectomesenchymal cells from the PAX3/SOX10/FOXD3-expressing MIXL1(-)CD271(hi)PDGFRα(lo)CD73(-) neural crest-like progeny of human pluripotent stem cells in a chemically defined medium supplemented with Nodal/Activin/transforming growth factorβ (TGFβ) inhibitor and fibroblast growth factor (FGF). When "primed" with TGFβ, such cells efficiently formed translucent cartilage particles, which were completely mineralized in 12 weeks in immunocompromized mice." [[Musculoskeletal System - Cartilage Development\|Cartilage Development]]

			* '''Just how conserved is vertebrate sex determination?'''{{#pmid:23390004\|PMID23390004}} "Sex determination in vertebrate embryos has long been equated with gonadal differentiation into testes or ovaries. This view has been challenged over the years by reports of somatic sexual dimorphisms pre-dating gonadal sex differentiation. ...We illustrate these differences by comparing key sex genes in fishes versus birds and mammals, with emphasis on DM domain genes, the SOX-9AMH pathway in the testis and the FOXL2-Aromatase pathway in the ovary. Such comparisons facilitate the identification of ancient versus derived genes involved in gonadal sex determination. The data indicate that vertebrate sex-determining cascades are not as conserved as once thought."

	* '''Sox2 is essential for formation of trophectoderm in the preimplantation embryo'''{{#pmid:21103067\|PMID21103067}} "In preimplantation mammalian development the transcription factor Sox2 (SRY-related HMG-box gene 2) forms a complex with Oct4 and functions in maintenance of self-renewal of the pluripotent inner cell mass (ICM). ...We conclude that the first essential function of Sox2 in the preimplantation mouse embryo is to facilitate establishment of the trophectoderm lineage. Our findings provide a novel insight into the first differentiation event within the preimplantation embryo, namely the segregation of the ICM and TE lineages."		* '''Sox2 is essential for formation of trophectoderm in the preimplantation embryo'''{{#pmid:21103067\|PMID21103067}} "In preimplantation mammalian development the transcription factor Sox2 (SRY-related HMG-box gene 2) forms a complex with Oct4 and functions in maintenance of self-renewal of the pluripotent inner cell mass (ICM). ...We conclude that the first essential function of Sox2 in the preimplantation mouse embryo is to facilitate establishment of the trophectoderm lineage. Our findings provide a novel insight into the first differentiation event within the preimplantation embryo, namely the segregation of the ICM and TE lineages."
	\|}		\|}

Z8600021 at 00:20, 7 November 2019

2019-11-07T00:20:50Z

← Older revision		Revision as of 10:20, 7 November 2019
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			* '''Sequence alteration in the enhancer contributes to the heterochronic {{Sox}}9 expression in marsupial cranial {{neural crest}}'''{{#pmid:31430446\|PMID31430446}} "Neonates of marsupial mammals are altricial at birth, because their gestation period is relatively short compared to placental mammals. Yet, as they need to travel to the teat from the birth canal, and suckle on the mother's milk, forelimbs and jaws develop significantly early. Previous studies in opossum (Monodelphis domestica), an experimental marsupial model, have revealed that cranial {{neural crest}} cells are generated significantly early compared to those in placental mammals, such as mouse, leading to an early development of jaw primordia. We have previously found that {{Sox}}9, an important neural crest-specifier gene, is expressed in the future cranial neural crest of the {{opossum}} embryonic ectoderm significantly earlier than that in mouse or quail embryos. As Sox9 is essential for neural crest formation in various vertebrates, it seems likely that the heterochronic expression of Sox9 is critical for the early cranial neural crest formation in the marsupial embryos. In this study, we show a marsupial-specific sequence in the Sox9 neural crest enhancer E3. We also reveal that the mouse E3 enhancer is activated in the cranial neural crest cells of quail embryos, that the E3 enhancer with marsupial-specific sequence is activated earlier in the Pax7-expressing neural border prior to the onset of endogenous Sox9 expression, and that a misexpression of cMyb, which is also a transcriptional activator of {{Pax}}7, in the neural border can ectopically activate the "marsupialized" enhancer. Thus, we suggest that the modification of the E3 enhancer sequence in the marsupial ancestor would have promoted the early expression of Sox9 in the neural border, facilitating the early formation of the cranial neural crest cells and the subsequent heterochronic development of the jaw primordia."

	* '''Prenatal Ascertainment of a Fetus With Homozygous Loss of the SOX10 Gene and Phenotypic Correlation by Autopsy Examination''' {{#pmid:29216801\|PMID29216801}} "The SOX10 gene plays a vital role in neural crest cell development and migration. Abnormalities in SOX10 are associated with Waardenburg syndrome Types II and IV, and these patients have recognizable clinical features. This case report highlights the first ever reported homozygous loss of function of the SOX10 gene in a human. This deletion is correlated using family history, prenatal ultrasound, microarray analysis of amniotic fluid, and ultimately, a medical autopsy examination to further elucidate phenotypic effects of this genetic variation." (More? {{Neural crest abnormalities}})		* '''Prenatal Ascertainment of a Fetus With Homozygous Loss of the SOX10 Gene and Phenotypic Correlation by Autopsy Examination''' {{#pmid:29216801\|PMID29216801}} "The SOX10 gene plays a vital role in neural crest cell development and migration. Abnormalities in SOX10 are associated with Waardenburg syndrome Types II and IV, and these patients have recognizable clinical features. This case report highlights the first ever reported homozygous loss of function of the SOX10 gene in a human. This deletion is correlated using family history, prenatal ultrasound, microarray analysis of amniotic fluid, and ultimately, a medical autopsy examination to further elucidate phenotypic effects of this genetic variation." (More? {{Neural crest abnormalities}})

Z8600021 at 01:24, 2 Mayıs 2019

2019-05-02T01:24:01Z

← Older revision		Revision as of 11:24, 2 Mayıs 2019
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	\|-bgcolor="F5FAFF"		\|-bgcolor="F5FAFF"
	\|		\|
	* '''Prenatal Ascertainment of a Fetus With Homozygous Loss of the SOX10 Gene and Phenotypic Correlation by Autopsy Examination''' {{#pmid:29216801\|PMID29216801}} "The SOX10 gene plays a vital role in neural crest cell development and migration. Abnormalities in SOX10 are associated with Waardenburg syndrome Types II and IV, and these patients have recognizable clinical features. This case report highlights the first ever reported homozygous loss of function of the SOX10 gene in a human. This deletion is correlated using family history, prenatal ultrasound, microarray analysis of amniotic fluid, and ultimately, a medical autopsy examination to further elucidate phenotypic effects of this genetic variation." (More? [[Neural ~~Crest System - Abnormalities\|Neural Crest Abnormalities]]~~)		* '''Prenatal Ascertainment of a Fetus With Homozygous Loss of the SOX10 Gene and Phenotypic Correlation by Autopsy Examination''' {{#pmid:29216801\|PMID29216801}} "The SOX10 gene plays a vital role in neural crest cell development and migration. Abnormalities in SOX10 are associated with Waardenburg syndrome Types II and IV, and these patients have recognizable clinical features. This case report highlights the first ever reported homozygous loss of function of the SOX10 gene in a human. This deletion is correlated using family history, prenatal ultrasound, microarray analysis of amniotic fluid, and ultimately, a medical autopsy examination to further elucidate phenotypic effects of this genetic variation." (More? {{Neural crest abnormalities}})

	* '''Distinct SoxB1 networks are required for naïve and primed pluripotency'''{{#pmid:29256862\|PMID29256862}} "Deletion of Sox2 from mouse embryonic stem cells (ESCs) causes trophectodermal differentiation. While this can be prevented by enforced expression of the related SOXB1 proteins, SOX1 or SOX3, the roles of SOXB1 proteins in epiblast stem cell (EpiSC) pluripotency are unknown. Here, we show that Sox2 can be deleted from EpiSCs with impunity. This is due to a shift in the balance of SoxB1 expression in EpiSCs, which have decreased Sox2 and increased Sox3 compared to ESCs. Consistent with functional redundancy, Sox3 can also be deleted from EpiSCs without eliminating self-renewal. However, deletion of both Sox2 and Sox3 prevents self-renewal. The overall SOXB1 levels in ESCs affect differentiation choices: neural differentiation of Sox2 heterozygous ESCs is compromised, while increased SOXB1 levels divert the ESC to EpiSC transition towards neural differentiation. Therefore, optimal SOXB1 levels are critical for each pluripotent state and for cell fate decisions during exit from naïve pluripotency." [[Stem Cells]]		* '''Distinct SoxB1 networks are required for naïve and primed pluripotency'''{{#pmid:29256862\|PMID29256862}} "Deletion of Sox2 from mouse embryonic stem cells (ESCs) causes trophectodermal differentiation. While this can be prevented by enforced expression of the related SOXB1 proteins, SOX1 or SOX3, the roles of SOXB1 proteins in epiblast stem cell (EpiSC) pluripotency are unknown. Here, we show that Sox2 can be deleted from EpiSCs with impunity. This is due to a shift in the balance of SoxB1 expression in EpiSCs, which have decreased Sox2 and increased Sox3 compared to ESCs. Consistent with functional redundancy, Sox3 can also be deleted from EpiSCs without eliminating self-renewal. However, deletion of both Sox2 and Sox3 prevents self-renewal. The overall SOXB1 levels in ESCs affect differentiation choices: neural differentiation of Sox2 heterozygous ESCs is compromised, while increased SOXB1 levels divert the ESC to EpiSC transition towards neural differentiation. Therefore, optimal SOXB1 levels are critical for each pluripotent state and for cell fate decisions during exit from naïve pluripotency." [[Stem Cells]]
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	* '''Long-term expandable SOX9+ chondrogenic ectomesenchymal cells from human pluripotent stem cells'''{{#pmid:25818812\|PMID25818812}} "Here we report the successful generation and long-term expansion of SOX9-expressing CD271(+)PDGFRα(+)CD73(+) chondrogenic ectomesenchymal cells from the PAX3/SOX10/FOXD3-expressing MIXL1(-)CD271(hi)PDGFRα(lo)CD73(-) neural crest-like progeny of human pluripotent stem cells in a chemically defined medium supplemented with Nodal/Activin/transforming growth factorβ (TGFβ) inhibitor and fibroblast growth factor (FGF). When "primed" with TGFβ, such cells efficiently formed translucent cartilage particles, which were completely mineralized in 12 weeks in immunocompromized mice." [[Musculoskeletal System - Cartilage Development\|Cartilage Development]]		* '''Long-term expandable SOX9+ chondrogenic ectomesenchymal cells from human pluripotent stem cells'''{{#pmid:25818812\|PMID25818812}} "Here we report the successful generation and long-term expansion of SOX9-expressing CD271(+)PDGFRα(+)CD73(+) chondrogenic ectomesenchymal cells from the PAX3/SOX10/FOXD3-expressing MIXL1(-)CD271(hi)PDGFRα(lo)CD73(-) neural crest-like progeny of human pluripotent stem cells in a chemically defined medium supplemented with Nodal/Activin/transforming growth factorβ (TGFβ) inhibitor and fibroblast growth factor (FGF). When "primed" with TGFβ, such cells efficiently formed translucent cartilage particles, which were completely mineralized in 12 weeks in immunocompromized mice." [[Musculoskeletal System - Cartilage Development\|Cartilage Development]]
	* '''Just how conserved is vertebrate sex determination?'''<ref name="PMID23390004"><pubmed>23390004</pubmed></ref> "Sex determination in vertebrate embryos has long been equated with gonadal differentiation into testes or ovaries. This view has been challenged over the years by reports of somatic sexual dimorphisms pre-dating gonadal sex differentiation. ...We illustrate these differences by comparing key sex genes in fishes versus birds and mammals, with emphasis on DM domain genes, the SOX-9AMH pathway in the testis and the FOXL2-Aromatase pathway in the ovary. Such comparisons facilitate the identification of ancient versus derived genes involved in gonadal sex determination. The data indicate that vertebrate sex-determining cascades are not as conserved as once thought."		* '''Just how conserved is vertebrate sex determination?'''<ref name="PMID23390004"><pubmed>23390004</pubmed></ref> "Sex determination in vertebrate embryos has long been equated with gonadal differentiation into testes or ovaries. This view has been challenged over the years by reports of somatic sexual dimorphisms pre-dating gonadal sex differentiation. ...We illustrate these differences by comparing key sex genes in fishes versus birds and mammals, with emphasis on DM domain genes, the SOX-9AMH pathway in the testis and the FOXL2-Aromatase pathway in the ovary. Such comparisons facilitate the identification of ancient versus derived genes involved in gonadal sex determination. The data indicate that vertebrate sex-determining cascades are not as conserved as once thought."

	* '''Sox2 is essential for formation of trophectoderm in the preimplantation embryo'''{{#pmid:21103067\|PMID21103067}} "In preimplantation mammalian development the transcription factor Sox2 (SRY-related HMG-box gene 2) forms a complex with Oct4 and functions in maintenance of self-renewal of the pluripotent inner cell mass (ICM). ...We conclude that the first essential function of Sox2 in the preimplantation mouse embryo is to facilitate establishment of the trophectoderm lineage. Our findings provide a novel insight into the first differentiation event within the preimplantation embryo, namely the segregation of the ICM and TE lineages."

	\|}		\|}
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	Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Sox+Expression ''Sox Expression'']		Search term: [http://www.ncbi.nlm.nih.gov/pubmed/?term=Sox+Expression ''Sox Expression'']
			\|}
	~~<pubmed limit~~=~~5>Sox Expression</pubmed>~~		{\| class="wikitable mw-collapsible mw-collapsed"
			! Older papers
			\|-
			\| {{Older papers}}
			* '''Sox2 is essential for formation of trophectoderm in the preimplantation embryo'''{{#pmid:21103067\|PMID21103067}} "In preimplantation mammalian development the transcription factor Sox2 (SRY-related HMG-box gene 2) forms a complex with Oct4 and functions in maintenance of self-renewal of the pluripotent inner cell mass (ICM). ...We conclude that the first essential function of Sox2 in the preimplantation mouse embryo is to facilitate establishment of the trophectoderm lineage. Our findings provide a novel insight into the first differentiation event within the preimplantation embryo, namely the segregation of the ICM and TE lineages."
	\|}		\|}
	==Human SOX Family==		==Human SOX Family==

Z8600021 at 02:33, 21 Mayıs 2018

2018-05-21T02:33:30Z

← Older revision		Revision as of 12:33, 21 Mayıs 2018
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	* Forms a trimeric transcription complex with OCT4.		* Forms a trimeric transcription complex with OCT4.
	* Gene targets - YES1, FGF4, UTF1 and ZFP206.		* Gene targets - YES1, FGF4, UTF1 and ZFP206.
			<br>
	{\|		{\|
	\|-bgcolor="CEDFF2"		\|-bgcolor="CEDFF2"

Z8600021 at 02:32, 21 Mayıs 2018

2018-05-21T02:32:48Z

@@ Line 53: / Line 53: @@
 * Forms a trimeric transcription complex with OCT4.
 * Gene targets - YES1, FGF4, UTF1 and ZFP206.
 | [[File:Mouse- embryonic stem cell signaling regulation.jpg|300px]]

Z8600021 at 02:30, 21 Mayıs 2018

2018-05-21T02:30:51Z

← Older revision		Revision as of 12:30, 21 Mayıs 2018
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	===SOX2===		===SOX2===
	~~[[File:Mouse- embryonic stem cell signaling regulation.jpg~~\|~~thumb~~\|~~Embryonic stem cell signaling SOX2]]~~		{\|
			\|
	* Sox2 is first expressed in very early (morula, blastocyst) development.		* Sox2 is first expressed in very early (morula, blastocyst) development.
	* Forms a trimeric transcription complex with OCT4.		* Forms a trimeric transcription complex with OCT4.
	* Gene targets - YES1, FGF4, UTF1 and ZFP206.		* Gene targets - YES1, FGF4, UTF1 and ZFP206.
			\| [[File:Mouse- embryonic stem cell signaling regulation.jpg\|300px]]

			Embryonic stem cell signaling SOX2
			\|}
	===SOX9===		===SOX9===
	[[File:Adrenal and gonad early development.jpg]]		[[File:Adrenal and gonad early development.jpg]]

Z8600021 at 02:29, 21 Mayıs 2018

2018-05-21T02:29:22Z

← Older revision		Revision as of 12:29, 21 Mayıs 2018
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	{{Sox family collapsetable}}		{{Sox family collapsetable}}

	==SOX2==		===SOX2===
			[[File:Mouse- embryonic stem cell signaling regulation.jpg\|thumb\|Embryonic stem cell signaling SOX2]]
			* Sox2 is first expressed in very early (morula, blastocyst) development.
			* Forms a trimeric transcription complex with OCT4.
			* Gene targets - YES1, FGF4, UTF1 and ZFP206.


	===SOX9===		===SOX9===

Z8600021 at 02:22, 21 Mayıs 2018

2018-05-21T02:22:20Z

← Older revision		Revision as of 12:22, 21 Mayıs 2018
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	<br>		<br>
	{{Sox family collapsetable}}		{{Sox family collapsetable}}

			==SOX2==

	===SOX9===		===SOX9===
			[[File:Adrenal and gonad early development.jpg]]


			SOX9 adrenal and gonad early development{{#pmid:14594453\|PMID14594453}}{{#pmid:29740094\|PMID29740094}}


	{\|		{\|
	\|-		\|-
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	\| [https://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=11204 SOX9] \|\| SRY-box 9 \|\| "CMD1, CMPD1" \|\| SRA1 \|\| [[:File:Human idiogram-chromosome 17.jpg\|17]]q24.3		\| [https://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=11204 SOX9] \|\| SRY-box 9 \|\| "CMD1, CMPD1" \|\| SRA1 \|\| [[:File:Human idiogram-chromosome 17.jpg\|17]]q24.3
	\|}		\|}

	~~[[File:Adrenal and gonad early development.jpg]]~~

	~~SOX9 adrenal and gonad early development{{#pmid:14594453\|PMID14594453}}~~

	==Early Mouse Expression==		==Early Mouse Expression==

Z8600021 at 02:18, 21 Mayıs 2018

2018-05-21T02:18:33Z

← Older revision		Revision as of 12:18, 21 Mayıs 2018
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	==Introduction==		==Introduction==
	[[File:Mouse-E10.5_ganglia_Sox10.jpg\|thumb\|Mouse (E10.5) Sox10 expression{{#pmid:20704721\|PMID20704721}}]]		[[File:Mouse-E10.5_ganglia_Sox10.jpg\|thumb\|Mouse (E10.5) Sox10 expression{{#pmid:20704721\|PMID20704721}}]]
	The SRY (480000) and SOX proteins share a DNA-binding domain known as the HMG box, defined by a 79-amino acid region.		The SRY (480000) and {{SOX}} proteins share a DNA-binding domain known as the HMG box, defined by a 79-amino acid region.