SCL/TAL1: a multifaceted regulator from blood development to disease
SCL/TAL1 (stem cell leukemia/T-cell acute lymphoblastic leukemia [T-ALL] 1) is an essential transcription factor in normal and malignant hematopoiesis. It is required for specification of the blood program during development, adult hematopoietic stem cell survival and quiescence, and terminal matura...
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| Veröffentlicht in: | Blood 2017-04, Vol.129 (15), p.2051-2060 |
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| creator | Porcher, Catherine Chagraoui, Hedia Kristiansen, Maiken S. |
| description | SCL/TAL1 (stem cell leukemia/T-cell acute lymphoblastic leukemia [T-ALL] 1) is an essential transcription factor in normal and malignant hematopoiesis. It is required for specification of the blood program during development, adult hematopoietic stem cell survival and quiescence, and terminal maturation of select blood lineages. Following ectopic expression, SCL contributes to oncogenesis in T-ALL. Remarkably, SCL's activities are all mediated through nucleation of a core quaternary protein complex (SCL:E-protein:LMO1/2 [LIM domain only 1 or 2]:LDB1 [LIM domain-binding protein 1]) and dynamic recruitment of conserved combinatorial associations of additional regulators in a lineage- and stage-specific context. The finely tuned control of SCL's regulatory functions (lineage priming, activation, and repression of gene expression programs) provides insight into fundamental developmental and transcriptional mechanisms, and highlights mechanistic parallels between normal and oncogenic processes. Importantly, recent discoveries are paving the way to the development of innovative therapeutic opportunities in SCL+ T-ALL. |
| doi_str_mv | 10.1182/blood-2016-12-754051 |
| format | Article |
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It is required for specification of the blood program during development, adult hematopoietic stem cell survival and quiescence, and terminal maturation of select blood lineages. Following ectopic expression, SCL contributes to oncogenesis in T-ALL. Remarkably, SCL's activities are all mediated through nucleation of a core quaternary protein complex (SCL:E-protein:LMO1/2 [LIM domain only 1 or 2]:LDB1 [LIM domain-binding protein 1]) and dynamic recruitment of conserved combinatorial associations of additional regulators in a lineage- and stage-specific context. The finely tuned control of SCL's regulatory functions (lineage priming, activation, and repression of gene expression programs) provides insight into fundamental developmental and transcriptional mechanisms, and highlights mechanistic parallels between normal and oncogenic processes. 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It is required for specification of the blood program during development, adult hematopoietic stem cell survival and quiescence, and terminal maturation of select blood lineages. Following ectopic expression, SCL contributes to oncogenesis in T-ALL. Remarkably, SCL's activities are all mediated through nucleation of a core quaternary protein complex (SCL:E-protein:LMO1/2 [LIM domain only 1 or 2]:LDB1 [LIM domain-binding protein 1]) and dynamic recruitment of conserved combinatorial associations of additional regulators in a lineage- and stage-specific context. The finely tuned control of SCL's regulatory functions (lineage priming, activation, and repression of gene expression programs) provides insight into fundamental developmental and transcriptional mechanisms, and highlights mechanistic parallels between normal and oncogenic processes. Importantly, recent discoveries are paving the way to the development of innovative therapeutic opportunities in SCL+ T-ALL.</description><subject>Adaptor Proteins, Signal Transducing - biosynthesis</subject><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Animals</subject><subject>Basic Helix-Loop-Helix Transcription Factors - genetics</subject><subject>Basic Helix-Loop-Helix Transcription Factors - metabolism</subject><subject>DNA-Binding Proteins - biosynthesis</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Gene Expression Regulation, Leukemic</subject><subject>Hematopoiesis</subject><subject>Hematopoietic Stem Cells - metabolism</subject><subject>Hematopoietic Stem Cells - pathology</subject><subject>Humans</subject><subject>LIM Domain Proteins - biosynthesis</subject><subject>LIM Domain Proteins - genetics</subject><subject>Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics</subject><subject>Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - metabolism</subject><subject>Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - pathology</subject><subject>Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - therapy</subject><subject>Proto-Oncogene Proteins - biosynthesis</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>T-Cell Acute Lymphocytic Leukemia Protein 1</subject><subject>Transcription Factors - biosynthesis</subject><subject>Transcription Factors - genetics</subject><issn>0006-4971</issn><issn>1528-0020</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtOwzAQRS0EgvL4A4SyZBOYce04YYGEylOqxIKythx7jIKSuthJJf6e0AJLNjObe-doDmOnCBeIJb-s2xBczgGLHHmupACJO2yCkpc5AIddNgGAIheVwgN2mNI7AIopl_vsgJeoqnFM2O3LbH65uJnjVWaybmj7xhtLPbks0tvQmj7EzMfQZRtc5mhNbVh1tOyzPmSuSWQSHbM9b9pEJz_7iL3e3y1mj_n8-eFpdjPPrVCizwszMg14WyuOypsaKpxCLR1yycG5gnsubG1VhUIZr6ByJMmB9NZbFG56xM63d1cxfAyUet01yVLbmiWFIWksi6KoprJUY1RsozaGlCJ5vYpNZ-KnRtDf_vTmIf3tTyPXW39j7eyHMNQdub_Sr7AxcL0N0PjnuqGok21oack1kWyvXWj-J3wBCQWAzQ</recordid><startdate>20170413</startdate><enddate>20170413</enddate><creator>Porcher, Catherine</creator><creator>Chagraoui, Hedia</creator><creator>Kristiansen, Maiken S.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-9015-5203</orcidid></search><sort><creationdate>20170413</creationdate><title>SCL/TAL1: a multifaceted regulator from blood development to disease</title><author>Porcher, Catherine ; Chagraoui, Hedia ; Kristiansen, Maiken S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-6a928a0fcb7217fab09130b5d12520dd62f24cbc79147af709de5ed05fcfc14d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adaptor Proteins, Signal Transducing - biosynthesis</topic><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Animals</topic><topic>Basic Helix-Loop-Helix Transcription Factors - genetics</topic><topic>Basic Helix-Loop-Helix Transcription Factors - metabolism</topic><topic>DNA-Binding Proteins - biosynthesis</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Gene Expression Regulation, Leukemic</topic><topic>Hematopoiesis</topic><topic>Hematopoietic Stem Cells - metabolism</topic><topic>Hematopoietic Stem Cells - pathology</topic><topic>Humans</topic><topic>LIM Domain Proteins - biosynthesis</topic><topic>LIM Domain Proteins - genetics</topic><topic>Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics</topic><topic>Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - metabolism</topic><topic>Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - pathology</topic><topic>Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - therapy</topic><topic>Proto-Oncogene Proteins - biosynthesis</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>T-Cell Acute Lymphocytic Leukemia Protein 1</topic><topic>Transcription Factors - biosynthesis</topic><topic>Transcription Factors - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Porcher, Catherine</creatorcontrib><creatorcontrib>Chagraoui, Hedia</creatorcontrib><creatorcontrib>Kristiansen, Maiken S.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Blood</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Porcher, Catherine</au><au>Chagraoui, Hedia</au><au>Kristiansen, Maiken S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SCL/TAL1: a multifaceted regulator from blood development to disease</atitle><jtitle>Blood</jtitle><addtitle>Blood</addtitle><date>2017-04-13</date><risdate>2017</risdate><volume>129</volume><issue>15</issue><spage>2051</spage><epage>2060</epage><pages>2051-2060</pages><issn>0006-4971</issn><eissn>1528-0020</eissn><abstract>SCL/TAL1 (stem cell leukemia/T-cell acute lymphoblastic leukemia [T-ALL] 1) is an essential transcription factor in normal and malignant hematopoiesis. It is required for specification of the blood program during development, adult hematopoietic stem cell survival and quiescence, and terminal maturation of select blood lineages. Following ectopic expression, SCL contributes to oncogenesis in T-ALL. Remarkably, SCL's activities are all mediated through nucleation of a core quaternary protein complex (SCL:E-protein:LMO1/2 [LIM domain only 1 or 2]:LDB1 [LIM domain-binding protein 1]) and dynamic recruitment of conserved combinatorial associations of additional regulators in a lineage- and stage-specific context. The finely tuned control of SCL's regulatory functions (lineage priming, activation, and repression of gene expression programs) provides insight into fundamental developmental and transcriptional mechanisms, and highlights mechanistic parallels between normal and oncogenic processes. Importantly, recent discoveries are paving the way to the development of innovative therapeutic opportunities in SCL+ T-ALL.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>28179281</pmid><doi>10.1182/blood-2016-12-754051</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-9015-5203</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - biosynthesis Adaptor Proteins, Signal Transducing - genetics Animals Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - metabolism DNA-Binding Proteins - biosynthesis DNA-Binding Proteins - genetics Gene Expression Regulation, Leukemic Hematopoiesis Hematopoietic Stem Cells - metabolism Hematopoietic Stem Cells - pathology Humans LIM Domain Proteins - biosynthesis LIM Domain Proteins - genetics Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - metabolism Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - pathology Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - therapy Proto-Oncogene Proteins - biosynthesis Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism T-Cell Acute Lymphocytic Leukemia Protein 1 Transcription Factors - biosynthesis Transcription Factors - genetics |
| title | SCL/TAL1: a multifaceted regulator from blood development to disease |
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