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HLF encodes a member of the proline and acidic-rich (PAR) protein family, a subset of the bZIP transcription factors. 再加上，我们可以发HLF 抗体 (46) 和 HLF 蛋白 (6)和数多这个蛋白质的别的产品。
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HLF-deficient hematopoietic stem cells display loss of quiescence and increased sensitivity to chemotoxic insults.
Results demonstrate that Hlf is a genetic modifier of epilepsy caused by voltage-gated sodium channel mutations and that modulation of the pyridoxine pathway can also influence phenotype severity
Conditional expression of E2A (显示 TCF3 ELISA试剂盒)-HLF induces B-cell precursor death and myeloproliferative-like disease in knock-in mice.
Data indicate that Meis homeobox 1 (MEIS1 (显示 MEIS1 ELISA试剂盒)) is required for the maintenance of myeloid-lymphoid leukemia protein MLL-fusion gene leukemia, and hepatic leukemia factor (HLF)is a key downstream mediator of Meis1 (显示 MEIS1 ELISA试剂盒).
we demonstrate that D site albumin promoter binding protein/thyrotroph embryonic factor (显示 TEF ELISA试剂盒)/hepatic leukemia factor triple knockout mice develop cardiac hypertrophy and left ventricular dysfunction associated with a low blood pressure
mice deficient for all three PAR bZip proteins (DBP,HLF,& TEF) are highly susceptible to generalized spontaneous and audiogenic epilepsies, frequently lethal. Pyridoxal kinase is a target gene of PAR bZip proteins in both liver and brain
The HLF protein control the expression of many enzymes and regulators involved in detoxification and drug metabolism, such as cytochrome P450 (显示 CYP ELISA试剂盒) enzymes, carboxylesterases, and constitutive androstane receptor (显示 NR1I3 ELISA试剂盒) (CAR).
Data show that the clock knockout mice or mice devoid of dbp (显示 GC ELISA试剂盒)/hlf/tef (显示 TEF ELISA试剂盒) (triple knockout) exhibit significant changes in renal expression of several key regulators of water or sodium balance.
Poly (ADP-ribose) polymerase (显示 PARP1 ELISA试剂盒) inhibitors selectively induce cytotoxicity in TCF3 (显示 TCF3 ELISA试剂盒)-HLF (显示 EPAS1 ELISA试剂盒)-positive leukemic cells.
HLF-mediated miR-132 directly suppresses TTK expression, thus exerting inhibitory effects on cancer cell proliferation, metastasis and radioresistance.
Drug response profiling of matched patient-derived xenografts revealed a distinct profile for TCF3 (显示 TCF3 ELISA试剂盒)-HLF (显示 EPAS1 ELISA试剂盒) ALL with resistance to conventional chemotherapeutics but sensitivity to glucocorticoids.
ectopic expression of HLF (显示 EPAS1 ELISA试剂盒), an established transcription factor that cycles with circadian rhythms, can recapitulate many features associated with circadian-dependent physiological variation.
both Lmo2 (显示 LMO2 ELISA试剂盒) and Bcl-2 (显示 BCL2 ELISA试剂盒) are required for the action of E2A (显示 TCF3 ELISA试剂盒)-HLF (显示 EPAS1 ELISA试剂盒) in leukemogenesis
E2A (显示 TCF3 ELISA试剂盒)-HLF (显示 EPAS1 ELISA试剂盒) promotes cell survival of t(17;19)- acute lymphoblastic leukemia cells by aberrantly up-regulating LMO2 (显示 LMO2 ELISA试剂盒) expression
Evidence pertaining to leukemogenesis by the well-characterized oncogenic fusion protein E2A (显示 TCF3 ELISA试剂盒)-HLF (显示 EPAS1 ELISA试剂盒) is reviewed and its mechanistic implications are considered.
E2A-HLF induces annexin II by substituting for cytokines that activate downstream pathways of Ras
The E2A (显示 TCF3 ELISA试剂盒)-HLF (显示 EPAS1 ELISA试剂盒)-mediated over-expression of ABCB1 (显示 ABCB1 ELISA试剂盒) may play a role in the clinical phenotype of ALLs with a t(17;19), suggesting pharmacologic modulation of ABCB1 (显示 ABCB1 ELISA试剂盒) activity as a rational therapeutic strategy for this chemotherapy resistant subtype of ALL.
The patients with immunophenotype of Pre-B-acute lymphoblastic leukemia were found to carry: E2A (显示 TCF3 ELISA试剂盒)/PBX1 (显示 PBX1 ELISA试剂盒) and E2A (显示 TCF3 ELISA试剂盒)/HLF (显示 EPAS1 ELISA试剂盒).
This gene encodes a member of the proline and acidic-rich (PAR) protein family, a subset of the bZIP transcription factors. The encoded protein forms homodimers or heterodimers with other PAR family members and binds sequence-specific promoter elements to activate transcription. Chromosomal translocations fusing portions of this gene with the E2A gene cause a subset of childhood B-lineage acute lymphoid leukemias. Alternatively spliced transcript variants have been described, but their biological validity has not been determined.
hepatic leukemia factor
, hepatic leukemia factor 1
, Hepatic leukemia factor