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NF-E2, TAL1 and KLF1, all activators play a primary role in HSs formation in the LCR
mutations of SF3B1 (show SF3B2 Proteins) may block erythropoiesis via dysregulation of alternative RNA splicing of transcription factor TAL1 (show TAL1 Proteins)
a novel role of FOXP3 (show FOXP3 Proteins) as a tumor suppressor in T-ALL through modulation of TAL1 (show TAL1 Proteins) transcriptional activity.
Review emphasizes recent findings that shed light into the intricacies of TAL1 (show TAL1 Proteins) (epi (show TFPI Proteins))genetic regulation and the transcription network orchestrated by this major T-cell oncogene (show RAB1A Proteins).[reiew]
Deletions of TAL1 (show TAL1 Proteins) is associated with acute T-lymphoblastic leukemia.
SCL/TAL1 (show TAL1 Proteins) (stem cell leukemia/T-cell acute lymphoblastic leukemia [T-ALL] 1) is an essential transcription factor in normal and malignant hematopoiesis.
Upregulation of TAL1 (show TAL1 Proteins) is associated with T-cell acute lymphoblastic leukemia.
Concurrent exogenous expression of three transcription factors, GATA1 (show GATA1 Proteins), FLI1 (show FLI1 Proteins) and TAL1 (show TAL1 Proteins), 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 (show HBG1 Proteins) includes a reduction in BCL11A (show BCL11A Proteins), KLF1 (show KLF1 Proteins) and TAL1 (show TAL1 Proteins) expression.
This study showed that Male mice lacking two key genes involved in Se metabolism (Scly(-/-)Sepp1 (show SEPP1 Proteins)(-/-) mice), selenoprotein P (Sepp1 (show SEPP1 Proteins)) and Sec lyase (Scly), develop severe neurological dysfunction, neurodegeneration, and audiogenic seizures.
our findings unveil a new metabolic role for Reg3beta in protein nitration and a new biosynthesis control of GPX1 (show GPX1 Proteins) by a completely "unrelated" regenerating protein, Reg3beta, via transcriptional activation of Scly
These findings provide the first in vivo evidence that Scly and Sepp1 (show SEPP1 Proteins) work cooperatively to maintain selenoprotein function in the mammalian brain.
The results suggested a dependence of glucose and lipid homeostasis on selenocysteine lyase activity. These findings connect Se and energy metabolism and demonstrate for the first time a unique physiological role of selenocysteine lyase.
Scly knockout mice do not display neurological dysfunction comparable to Sepp1 (show SEPP1 Proteins) knockout mice.
Selenocysteine lyase (SCLY\; EC 18.104.22.168) catalyzes the pyridoxal 5-prime phosphate-dependent conversion of L-selenocysteine to L-alanine and elemental selenium (Mihara et al., 2000
, Selenocysteine lyase
, selenocysteine lyase; Selenocysteine reductase
, selenocysteine reductase
, T-cell acute lymphocytic leukemia protein 1
, T-cell leukemia/lymphoma protein 5
, class A basic helix-loop-helix protein 17
, stem cell protein
, tal-1 product