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HLF encodes a member of the proline and acidic-rich (PAR) protein family, a subset of the bZIP transcription factors. Additionally we are shipping HLF Antibodies (44) and HLF Proteins (6) and many more products for this protein.
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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 (show TCF3 ELISA Kits)-HLF induces B-cell precursor death and myeloproliferative-like disease in knock-in mice.
Data indicate that Meis homeobox 1 (MEIS1 (show MEIS1 ELISA Kits)) 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 (show MEIS1 ELISA Kits).
we demonstrate that D site albumin promoter binding protein/thyrotroph embryonic factor (show TEF ELISA Kits)/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 (show CYP ELISA Kits) enzymes, carboxylesterases, and constitutive androstane receptor (show NR1I3 ELISA Kits) (CAR).
Data show that the clock knockout mice or mice devoid of dbp (show GC ELISA Kits)/hlf/tef (show TEF ELISA Kits) (triple knockout) exhibit significant changes in renal expression of several key regulators of water or sodium balance.
Poly (ADP-ribose) polymerase (show PARP1 ELISA Kits) inhibitors selectively induce cytotoxicity in TCF3 (show TCF3 ELISA Kits)-HLF (show EPAS1 ELISA Kits)-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 (show TCF3 ELISA Kits)-HLF (show EPAS1 ELISA Kits) ALL with resistance to conventional chemotherapeutics but sensitivity to glucocorticoids.
ectopic expression of HLF (show EPAS1 ELISA Kits), an established transcription factor that cycles with circadian rhythms, can recapitulate many features associated with circadian-dependent physiological variation.
both Lmo2 (show LMO2 ELISA Kits) and Bcl-2 (show BCL2 ELISA Kits) are required for the action of E2A (show TCF3 ELISA Kits)-HLF (show EPAS1 ELISA Kits) in leukemogenesis
E2A (show TCF3 ELISA Kits)-HLF (show EPAS1 ELISA Kits) promotes cell survival of t(17;19)- acute lymphoblastic leukemia cells by aberrantly up-regulating LMO2 (show LMO2 ELISA Kits) expression
Evidence pertaining to leukemogenesis by the well-characterized oncogenic fusion protein E2A (show TCF3 ELISA Kits)-HLF (show EPAS1 ELISA Kits) 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 (show TCF3 ELISA Kits)-HLF (show EPAS1 ELISA Kits)-mediated over-expression of ABCB1 (show ABCB1 ELISA Kits) may play a role in the clinical phenotype of ALLs with a t(17;19), suggesting pharmacologic modulation of ABCB1 (show ABCB1 ELISA Kits) 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 (show TCF3 ELISA Kits)/PBX1 (show PBX1 ELISA Kits) and E2A (show TCF3 ELISA Kits)/HLF (show EPAS1 ELISA Kits).
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