Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Weitere Synonyme anzeigen
Wählen Sie die gewünschte Spezies
Study reveals a complex pattern of gene regulation by SCL, ETO2 and RYBP. Genome-wide analyses shows locus-specific binding of ETO2 and RYBP on SCL's 778 activated and repressed genes.
Tal1 plays an essential role in regulating neurotransmitter phenotype in the developing thalamic nuclei.
Genome-wide analysis indicated that LMO2 is required at the hemangioblast stage to position the TAL1/LMO2/LDB1 complex to regulatory elements that are important for the establishment of the hematopoietic developmental program.
TAL1 and GATA1 form a precisely organized complex at a compound motif consisting of a TG 7 or 8 bp upstream of a WGATAA motif across thousands of genomic locations
SCL-LMO1 upregulated a stem cell gene signature in DN3 thymocytes.
TAL1 binds specifically to many genomic locations in multilineage precursor and erythroid progenitor cells, before GATA1 is produced abundantly.
Ectopic Runx1 expression rescues Tal-1-deficiency in the generation of primitive and definitive hematopoiesis.
Tal1 has a role in severe renal disease and patchy alopecia in Hairpatches (Hpt) mice
Only Scl but not Map17 could rescue the Scl(Delta40/Delta40) ES phenotype.
Scl overexpression is sufficient to rescue the developmental defects caused by blocking the Hh and Notch pathways during the embryonic endothelial-to-hematopoietic transition.
a novel role for GATA-4 and TAL1 to affect skeletal myogenic differentiation and EPO response via cross-talk with Sirt1.
Studies revealed an unexpected repressive role for Scl, as loss of Scl resulted in the generation of ectopic cardiomyocytes in yolk sac vasculature and the endocardium; these results uncover remarkable developmental plasticity in embryonic vasculature and identify Scl as a key determinant of endothelial fate choice.
Deletion of the Scl +19 enhancer increases the blood stem cell compartment without affecting the formation of mature blood lineages.
characterisation of a CTCF-dependent insulator element at the 3' border of the murine Scl transcriptional domain
GATA-1, SCL, and Klf1 form an erythroid core transcriptional network by co-occupying >300 genes
found that DC-STAMP, a key regulator of osteoclast cell fusion, is a direct target gene of Tal1 and show that Tal1 represses DC-STAMP expression by counteracting the activating function of the transcription factors PU.1 and MITF
Data show that thymic expression of the Tal1 and Lmo2 oncogenes results in rapid development of T-ALL, and similar to T-ALL patients, more than half the leukemic mice develop spontaneous mutations in Notch1.
SCL-mediated transcriptional control of p21 is essential for terminal maturation of megakaryopoiesis
DNA-binding activity of Tal1 is not required to cooperate with Lmo2 to cause leukemia in mice
TAL1 coordinates expression of genes in most known red cell-specific processes. Novel motifs were also characterized that may help distinguish activated from repressed genes and suggest a new mechanism by which TAL1 may be recruited to DNA.
TAL1 mediates the function of MEIS1 in hemogenic endothelial progenitors specification. In addition, MEIS1 is vital for megakaryopoiesis and thrombopoiesis from hPSCs. Mechanistically, FLI1 acts as a downstream gene necessary for the function of MEIS1 during megakaryopoiesis
HOPX is functionally regulated by SCL in hematoendothelial differentiation of mesoderm progenitor cells.
NF-E2, TAL1 and KLF1, all activators play a primary role in HSs formation in the LCR
mutations of SF3B1 may block erythropoiesis via dysregulation of alternative RNA splicing of transcription factor TAL1
a novel role of FOXP3 as a tumor suppressor in T-ALL through modulation of TAL1 transcriptional activity.
Review emphasizes recent findings that shed light into the intricacies of TAL1 (epi)genetic regulation and the transcription network orchestrated by this major T-cell oncogene.[reiew]
Deletions of TAL1 is associated with acute T-lymphoblastic leukemia.
SCL/TAL1 (stem cell leukemia/T-cell acute lymphoblastic leukemia [T-ALL] 1) is an essential transcription factor in normal and malignant hematopoiesis.
Upregulation of TAL1 is associated with T-cell acute lymphoblastic leukemia.
Concurrent exogenous expression of three transcription factors, GATA1, FLI1 and TAL1, enables large-scale production of megakaryocytes from human pluripotent stem cells.
analysis of a point mutation that increases fetal globin expression through de novo recruitment of the activator TAL1 to promote chromatin looping of distal enhancers to the modified gamma-globin promoter
a successful induction of gamma-globin includes a reduction in BCL11A, KLF1 and TAL1 expression.
SCL-mediated transcriptional network enhances megakaryocytic specification of human embryonic stem cells.
These results indicate that KLF1 plays a role in facilitating and/or stabilizing GATA-1 and TAL1 occupancy in the erythroid genes, contributing to the generation of active chromatin structure such as histone acetylation and chromatin looping
Scl binds to primed enhancers in mesoderm to regulate hematopoietic and cardiac fate divergence.
SCL/TAL1 is located in the up-stream of MEK/ERK pathway and partially regulates hematopoiesis by modulating the phosphorylation level of the key proteins in MEK/ERK pathway.
study found that heterozygous somatic mutations are acquired that introduce binding motifs for the MYB transcription factor in a precise noncoding site, which creates a super-enhancer upstream of the TAL1 oncogene; MYB binds to this new site
The results indicate that TAL1 plays a critical role in chromatin loop formation between the gamma-globin genes and locus control region, which is a critical step for the transcription of the gamma-globin genes.
SIL-TAL1 rearrangement identifies a distinct subtype with inferior outcome which could allow for individual therapeutic stratification for T-ALL patients.
our study reveals a novel molecular mechanism involving changes in three-dimensional chromatin interactions that activate the TAL1 oncogene in human T-cell leukemia.
The latter data suggest that Stil play a role in retina cell proliferation through the Shh signal transduction pathway.
Tal1 has distinct roles in regulating the formation of endocardial intercellular junctions.
Data suggest that a defined hemogenic endothelial population preset by scl-beta supports the deterministic emergence of HSCs, and unravel the cellular mechanisms by which scl isoforms regulate HSC development.
Our studies establish a new connection between RA and scl during development that may participate in stem cell self-renewal and hematopoietic differentiation
Ets1-related protein plays a critical role in the initiation of definitive hematopoiesis by controlling the expression of 2 stem cell leukemia (scl) isoforms (scl-alpha and scl-beta) in angioblasts.
in the absence of inducers of erythroid or myeloid haematopoiesis, Scl/Tal1-Lmo2-induced haemangioblasts differentiate into endothelial cells
Zebrafish scl has a role in hematopoietic and endothelial development, downstream of hemangioblast development.
scl is especially critical for the development of arteries where adult hematopoietic stem cells emerge, implicating scl in the formation of hemogenic endothelium
Scl participates in multiple processes requiring different levels and functions
While scl-alpha and -beta are redundant for the initiation of primitive hematopoiesis, these two isoforms exert distinct functions in the regulation of primitive erythroid differentiation and definitive hematopoietic stem cell specification.
In germline-transgenic zebrafish generated by inserting GFP into the first coding exon of scl, GFP expression completely recapitulates the endogenous expression of scl in blood, endothelium and CNS.
Scl/Tal1 is an indispensable component of the molecular hierarchy that controls endocardium morphogenesis.
These results demonstrate that scl is an important mediator of the ability of AML1-ETO to reprogram hematopoietic cell fate decisions, suggesting that scl may be an important contributor to AML1-ETO-associated leukemia.
the choice of endothelial versus myeloid fate depends on a combinatorial effect of etsrp, scl, and alk8 ge
Transcription factor that acts synergistically with lmo2 and gata1 to specify embryonic dorsal mesoderm to a hematopoietic fate.
T-cell acute lymphocytic leukemia 1
, T-cell acute lymphocytic leukemia protein 1 homolog
, stem cell protein
, T-cell acute lymphocytic leukemia protein 1
, T-cell leukemia/lymphoma protein 5
, class A basic helix-loop-helix protein 17
, tal-1 product
, stem cell leukaemia
, stem cell leukemia protein SCL
, Avian SCL
, stem-cell leukemia hematopoietic transcription factor
, transcription factor