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purified and functionally characterized the critical transcription factor HiNF-P, which is required for E2F-independent activation of the histone H4 multigene family
These results suggest that transcriptional repression of Rb by MIZF could be one of the critical determinants in myogenic differentiation.
HiNF-P interacts directly with p220(NPAT) to coactivate histone genes during S phase.
the transcriptional silencing of the 14-3-3sigma gene is caused by promoter CpG island methylation associated with MBD2 (Montrer DPEP2 Kits ELISA), which may play an important role in prostate cancer progression during the invasive and metastatic stages of the disease
These results suggest that RFP (Montrer FPR2 Kits ELISA) is a mediator connecting several MBD (Montrer DPEP1 Kits ELISA) proteins and allowing the formation of a more potent transcriptional repressor complex.
HiNF-P is a bifunctional regulator of cell cycle controlled histone H4 gene transcription.
HiNF-P-dependent stabilization of p220NPAT reinforces signaling through the cyclin E (Montrer CCNE1 Kits ELISA)/CDK2 (Montrer CDK2 Kits ELISA)/p220NPAT pathway and contributes to coordinate control of histone gene expression.
HiNF-P/P220NPAT regulates expression of nonhistone targets that influence competency for cell cycle progression.
a novel HiNF-P-specific conserved region represents a DNA-binding determinant that plays a role in mediating histone gene expression during the cell cycle and defines HiNF-P as a cell cycle regulatory member of the zinc finger transcription factor (Montrer OSR1 Kits ELISA) family
Results suggest that cyclin-dependent kinase inhibitors selectively control stimulation of the histone H4 gene promoter by the p220(NPAT)/HiNF-P complex.
Induction of Hinfp begins at the 4-cell stage. Maternally encoded Hinfp sustains development of pre-implantation stage embryos. Hinfp loss delays growth of blastocyst stage embryos that later fail to implant. Hinfp ablation severely reduces histone H4 mRNA and causes DNA damage. Transmission of maternal Hinfp transcripts and zygotic activation of the Hinfp gene together are neeeded to control early H4 gene expression.
simultaneous loss of both Hinfp and the p53 (Montrer TP53 Kits ELISA) checkpoint is detrimental to normal cell growth and may predispose to cellular transformation.
Data show that conditional ablation of HINFP compromises cell proliferation, impairs DNA synthesis, alters nucleosome spacing and increases double-stranded DNA damage.
The in vivo co-expression of Hinfp and histone H4 genes is consistent with the biological function of Hinfp as a principal transcriptional regulator of histone H4 gene expression during mouse development.
The dependence of HiNF-P gene transcription on cyclin E/CDK2/p220NPAT signaling defines a novel feed-forward loop that may sustain HiNF-P expression in proliferating cells to support the cell cycle regulated synthesis of histone H4 proteins.
Data indicate that the CDK2/cyclin E/p220(NPAT)/HINFP/histone gene signaling pathway at the G1/S phase transition is an essential, nonredundant cell cycle regulatory mechanism that is established early in embryogenesis.
This gene encodes a transcription factor that interacts with methyl-CpG-binding protein-2 (MBD2), a component of the MeCP1 histone deacetylase (HDAC) complex, and plays a role in DNA methylation and transcription repression. Alternatively spliced transcript variants have been found for this gene.
MBD2 (methyl-CpG-binding protein)-interacting zinc finger protein
, MBD2-interacting zinc finger 1
, MBD2-interacting zinc finger protein
, histone H4 gene-specific protein HiNF-P
, histone nuclear factor P
, methyl-CpG-binding protein 2-interacting zinc finger protein
, MBD2-interacting zinc finger