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HLF encodes a member of the proline and acidic-rich (PAR) protein family, a subset of the bZIP transcription factors. De plus, nous expédions HLF Anticorps (45) et HLF Protéines (6) et beaucoup plus de produits pour cette protéine.
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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 (Montrer TCF3 Kits ELISA)-HLF induces B-cell precursor death and myeloproliferative-like disease in knock-in mice.
Data indicate that Meis homeobox 1 (MEIS1 (Montrer MEIS1 Kits ELISA)) 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 (Montrer MEIS1 Kits ELISA).
we demonstrate that D site albumin promoter binding protein/thyrotroph embryonic factor (Montrer TEF Kits ELISA)/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 (Montrer CYP Kits ELISA) enzymes, carboxylesterases, and constitutive androstane receptor (Montrer NR1I3 Kits ELISA) (CAR).
Data show that the clock knockout mice or mice devoid of dbp (Montrer GC Kits ELISA)/hlf/tef (Montrer TEF Kits ELISA) (triple knockout) exhibit significant changes in renal expression of several key regulators of water or sodium balance.
Poly (ADP-ribose) polymerase (Montrer PARP1 Kits ELISA) inhibitors selectively induce cytotoxicity in TCF3 (Montrer TCF3 Kits ELISA)-HLF (Montrer EPAS1 Kits ELISA)-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 (Montrer TCF3 Kits ELISA)-HLF (Montrer EPAS1 Kits ELISA) ALL with resistance to conventional chemotherapeutics but sensitivity to glucocorticoids.
ectopic expression of HLF (Montrer EPAS1 Kits ELISA), an established transcription factor that cycles with circadian rhythms, can recapitulate many features associated with circadian-dependent physiological variation.
both Lmo2 (Montrer LMO2 Kits ELISA) and Bcl-2 (Montrer BCL2 Kits ELISA) are required for the action of E2A (Montrer TCF3 Kits ELISA)-HLF (Montrer EPAS1 Kits ELISA) in leukemogenesis
E2A (Montrer TCF3 Kits ELISA)-HLF (Montrer EPAS1 Kits ELISA) promotes cell survival of t(17;19)- acute lymphoblastic leukemia cells by aberrantly up-regulating LMO2 (Montrer LMO2 Kits ELISA) expression
Evidence pertaining to leukemogenesis by the well-characterized oncogenic fusion protein E2A (Montrer TCF3 Kits ELISA)-HLF (Montrer EPAS1 Kits ELISA) 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 (Montrer TCF3 Kits ELISA)-HLF (Montrer EPAS1 Kits ELISA)-mediated over-expression of ABCB1 (Montrer ABCB1 Kits ELISA) may play a role in the clinical phenotype of ALLs with a t(17;19), suggesting pharmacologic modulation of ABCB1 (Montrer ABCB1 Kits ELISA) 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 (Montrer TCF3 Kits ELISA)/PBX1 (Montrer PBX1 Kits ELISA) and E2A (Montrer TCF3 Kits ELISA)/HLF (Montrer EPAS1 Kits ELISA).
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