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uc.40 may play an important role during the differentiation of P19 cells by regulation of PBX1 to promote proliferation and inhibit apoptosis.
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Expression of PBX1 in leukemia cells enhances chemo-resistance and colony formation.
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Pbx-dependent Epithelial-mesenchymal transition programs mediate murine upper lip/primary palate morphogenesis and fusion via regulation of Snail1.
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MEIS2 associates with chromatin-bound PBX1, recruits PARP1/ARTD1, and initiates PARP1-mediated eviction of H1 from the chromatin fiber.
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results indicate Pbx genes act in parallel genetic pathways to orchestrate neuronal subtype differentiation, connectivity, and organization. I
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Hoxa2, Meis and Pbx proteins act cooperatively on the ECR, via a core 32 bp sequence, to regulate Hmx1 expression.
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PBX1 regulates adult neural cell fate determination in a manner beyond that of its heterodimerization partner MEIS2.
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Our results suggest that Pbx1-d impacts lupus development by regulating effector T cell differentiation and promoting follicular helper T cells at the expense of regulatory T cell s and identify Pbx1 as a novel regulator of CD4(+) T cell effector function
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FLT3-ITD is capable of inhibiting FLT3-ITD+ cell proliferation through the p21/Pbx1 axis
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non-cell autonomous functions of Pbx factors within the splenic niche contribute to the regulation of hematopoiesis
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Both histone H3 lysine 27 acetylation and recruitment of the transcription factor Pbx1 at prospective enhancers are regulated by mH2A1.2.
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Thus, PTBP1 controls the activity of Pbx1 to suppress its neuronal transcriptional program prior to induction of neuronal progenitor cells development.
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this study showed that the lupus susceptibility gene Pbx1 not only contributes to autoimmune pathology by impairing T cell tolerance, but also impairs the function of mesenchymal stem cells, which may also contribute to the disease directly or indirectly.
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Pbx1-dependent control of VMC differentiation kinetics underlies gross renal vascular patterning.
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Results thus show how Pbx1 controls Fgf10 in the developing lung.
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Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis.
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These results demonstrate a role for Pbx1 in restraining myeloid maturation while maintaining lymphoid potential to appropriately regulate progenitor reservoirs.
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The Systemic Lupus Erythematosus-associated Pbx1-d isoform acts as a dominant-negative transcriptional regulator.
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Data have demonstrated the presence of Meis, Pbx, and Prep proteins during early lineage segregation in mammals: Meis1, Meis3, Pbx1, Pbx2, Pbx3, and Prep1 in the mouse.
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In Pbx1-deficient dopaminergic neurons, the high affinity netrin-1 receptor, deleted in colon cancer, is down-regulated.