anti-Hepatic Leukemia Factor (HLF) Antibodies

Mouse (Murine) Hepatic Leukemia Factor (HLF) interaction partners

1. HLF-deficient hematopoietic stem cells display loss of quiescence and increased sensitivity to chemotoxic insults.

2. 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

3. Conditional expression of E2A-HLF induces B-cell precursor death and myeloproliferative-like disease in knock-in mice.

4. Data indicate that Meis homeobox 1 (MEIS1) 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.

5. we demonstrate that D site albumin promoter binding protein/thyrotroph embryonic factor/hepatic leukemia factor triple knockout mice develop cardiac hypertrophy and left ventricular dysfunction associated with a low blood pressure

6. 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

7. The HLF protein control the expression of many enzymes and regulators involved in detoxification and drug metabolism, such as cytochrome P450 enzymes, carboxylesterases, and constitutive androstane receptor (CAR).

8. Data show that the clock knockout mice or mice devoid of dbp/hlf/tef (triple knockout) exhibit significant changes in renal expression of several key regulators of water or sodium balance.

Human Hepatic Leukemia Factor (HLF) interaction partners

1. Poly (ADP-ribose) polymerase inhibitors selectively induce cytotoxicity in TCF3-HLF-positive leukemic cells.

2. HLF-mediated miR-132 directly suppresses TTK expression, thus exerting inhibitory effects on cancer cell proliferation, metastasis and radioresistance.

3. Drug response profiling of matched patient-derived xenografts revealed a distinct profile for TCF3-HLF ALL with resistance to conventional chemotherapeutics but sensitivity to glucocorticoids.

4. ectopic expression of HLF, an established transcription factor that cycles with circadian rhythms, can recapitulate many features associated with circadian-dependent physiological variation.

5. both Lmo2 and Bcl-2 are required for the action of E2A-HLF in leukemogenesis

6. E2A-HLF promotes cell survival of t(17;19)- acute lymphoblastic leukemia cells by aberrantly up-regulating LMO2 expression

7. Evidence pertaining to leukemogenesis by the well-characterized oncogenic fusion protein E2A-HLF is reviewed and its mechanistic implications are considered.

8. E2A-HLF induces annexin II by substituting for cytokines that activate downstream pathways of Ras

9. The E2A-HLF-mediated over-expression of ABCB1 may play a role in the clinical phenotype of ALLs with a t(17;19), suggesting pharmacologic modulation of ABCB1 activity as a rational therapeutic strategy for this chemotherapy resistant subtype of ALL.

10. The patients with immunophenotype of Pre-B-acute lymphoblastic leukemia were found to carry: E2A/PBX1 and E2A/HLF.

11. In childhood acute lymphoblastic leukemia and hypercalcemia, translocation was observed in E2A-HLF fusion protein.

12. Activation of the thyroid hormone receptor beta/retinoid X receptor alpha heterodimer by T(3) stimulated expression of the hepatic leukemia factor, which increases HIF-1alpha gene expression.

13. The authors characterize variants of rat HLF, including use of two alternative promoters and a non-AUG translation initiation site that has not been confirmed in human.