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Lymphoblastic leukemia derived sequence 1

This gene represents a basic helix-loop-helix transcription factor. The encoded protein may play roles in blood vessel maturation and hematopoeisis. A translocation between this locus and the T cell receptor beta locus (GeneID 6957) on chromosome 7 has been associated with acute lymphoblastic leukemia. [provided by RefSeq, Sep 2010] (from NCBI)
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Top mentioned proteins: CK7, LMO2, E12, CAN, LIM-only
Papers on LYL1
The oncofusion protein FUS-ERG targets key hematopoietic regulators and modulates the all-trans retinoic acid signaling pathway in t(16;21) acute myeloid leukemia.
Martens et al., Nijmegen, Netherlands. In Oncogene, Aug 2015
Here, we show that FUS-ERG acts in the context of a heptad of proteins (ERG, FLI1, GATA2, LYL1, LMO2, RUNX1 and TAL1) central to proper expression of genes involved in maintaining a stem cell hematopoietic phenotype.
A population-based single nucleotide polymorphism array analysis of genomic aberrations in younger adult acute lymphoblastic leukemia patients.
Griskevicius et al., Vilnius, Lithuania. In Genes Chromosomes Cancer, May 2015
ARHGEF12 in 11q23.3, and LYL1 in 19p13.2.
Expression of the potential therapeutic target CXXC5 in primary acute myeloid leukemia cells - high expression is associated with adverse prognosis as well as altered intracellular signaling and transcriptional regulation.
Pendino et al., Bergen, Norway. In Oncotarget, Mar 2015
High CXXC5 expression was also associated with high mRNA expression of several stem cell-associated transcriptional regulators, the strongest associations being with WT1, GATA2, RUNX1, LYL1, DNMT3, SPI1, and MYB.
Enforced expression of E47 has differential effects on Lmo2-induced T-cell leukemias.
Davé et al., Nashville, United States. In Leuk Res, 2015
In hematopoietic stem and progenitor cells, Lmo2 is part of a protein complex comprised of class II basic helix loop helix proteins, Tal1and Lyl1.
SCL, LMO1 and Notch1 reprogram thymocytes into self-renewing cells.
Hoang et al., Montréal, Canada. In Plos Genet, 2014
Second, we provide strong genetic evidence that SCL directly interacts with LMO1 to activate the transcription of a self-renewal program coordinated by LYL1.
Friend or foe: can activating mutations in NOTCH1 contribute to a favorable treatment outcome in patients with T-ALL?
Berger et al., Jerusalem, Israel. In Crit Rev Oncog, 2013
Transformation events occur during crucial steps of thymocyte development and have been related to the expression of certain oncogenes such as TAL2, TLX1, LYL1, LMO1, and NOTCH1.
The transcription factor Lyl-1 regulates lymphoid specification and the maintenance of early T lineage progenitors.
Goodell et al., Düsseldorf, Germany. In Nat Immunol, 2012
Lyl-1 is a pivotal component of a transcriptional program that controls the lymphoid specification and maintenance of early T lineage progenitors
Concise review: Blood relatives: formation and regulation of hematopoietic stem cells by the basic helix-loop-helix transcription factors stem cell leukemia and lymphoblastic leukemia-derived sequence 1.
Pimanda et al., Melbourne, Australia. In Stem Cells, 2012
In hematopoiesis, the two major bHLH factors are stem cell leukemia (SCL) and lymphoblastic leukemia-derived sequence 1 (LYL1), both identified more than 20 years ago in chromosomal translocations occurring in T-cell acute lymphoblastic leukemia.
LYL-1 deficiency induces a stress erythropoiesis.
Vainchenker et al., Villejuif, France. In Exp Hematol, 2011
results suggest that LYL-1 plays a definite role in erythropoiesis, albeit with different effects in bone marrow specifically regulating basal erythropoiesis, and spleen, controlling stress-induced erythropoiesis
The expansion of T-cells and hematopoietic progenitors as a result of overexpression of the lymphoblastic leukemia gene, Lyl1 can support leukemia formation.
Goodell et al., Houston, United States. In Leuk Res, 2011
Overexpression of Lyl1 is associated with leukemia formation.
Combinatorial transcriptional control in blood stem/progenitor cells: genome-wide analysis of ten major transcriptional regulators.
Göttgens et al., Cambridge, United Kingdom. In Cell Stem Cell, 2010
Here, we report the genome-wide binding patterns and combinatorial interactions for ten key regulators of blood stem/progenitor cells (SCL/TAL1, LYL1, LMO2, GATA2, RUNX1, MEIS1, PU.1, ERG, FLI-1, and GFI1B), thus providing the most comprehensive TF data set for any adult stem/progenitor cell type to date.
LYL1 activity is required for the maturation of newly formed blood vessels in adulthood.
Pinet et al., Montpellier, France. In Blood, 2010
LYL1 activity is required for the maturation of newly formed blood vessels in adulthood.
LYL1 degradation by the proteasome is directed by a N-terminal PEST rich site in a phosphorylation-independent manner.
Goodell et al., Houston, United States. In Plos One, 2009
LYL1 degradation is directed by a N-terminal PEST rich site in a phosphorylation-independent manner.
Adult hematopoietic stem and progenitor cells require either Lyl1 or Scl for survival.
Goodell et al., Houston, United States. In Cell Stem Cell, 2009
These results show that expression of Lyl1 or Scl is essential for maintenance of adult hematopoietic stem cell function.
Mechanisms of transcription factor deregulation in lymphoid cell transformation.
Look et al., Boston, United States. In Oncogene, 2007
TAL1, LYL1, HOX11 and other transcription factors essential for normal hematopoiesis are often misexpressed in the thymus in T-cell acute lymphoblastic leukemia (T-ALL), leading to differentiation arrest and cell transformation.
Prognostic importance of TLX1 (HOX11) oncogene expression in adults with T-cell acute lymphoblastic leukaemia.
Look et al., Boston, United States. In Lancet, 2004
We investigated the prognostic effect of the expression levels of eight oncogenic transcription factors--TLX1 (HOX11), TLX3 (HOX11L2), TAL1, TAL2, LYL1, OLIG2 (BHLHB1), LMO1, and LMO2--in 52 adults with T-cell acute lymphoblastic leukaemia.
Gene expression profiling in T-cell acute lymphoblastic leukemia.
Look et al., Boston, United States. In Semin Hematol, 2003
Five different multistep molecular pathways have been identified that lead to T-ALL, involving activation of different T-ALL oncogenes: (1) HOX11, (2) HOX11L2, (3) TAL1 plus LMO1/2, (4) LYL1 plus LMO2, and (5) MLL-ENL.
Gene expression signatures define novel oncogenic pathways in T cell acute lymphoblastic leukemia.
Look et al., Boston, United States. In Cancer Cell, 2002
Here we show that five different T cell oncogenes (HOX11, TAL1, LYL1, LMO1, and LMO2) are often aberrantly expressed in the absence of chromosomal abnormalities.
Absence of blood formation in mice lacking the T-cell leukaemia oncoprotein tal-1/SCL.
Orkin et al., Boston, United States. In Nature, 1995
In human T-cell leukaemias such regulators belong to diverse protein families and may normally be expressed widely (for example, Ttg-1/rbtn1, Ttg-2/rbtn2), exclusively outside the haematopoietic system (for example, Hox11), or specifically in haematopoietic cells and other selected sites (for example, tal-1/SCL, lyl-1).
TAL1, TAL2 and LYL1: a family of basic helix-loop-helix proteins implicated in T cell acute leukaemia.
Baer, Dallas, United States. In Semin Cancer Biol, 1993
The bHLH domain of TAL1 is especially homologous to those encoded by TAL2 and LYL1, distinct genes that were also identified on the basis of chromosomal rearrangement in T-ALL.
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