Target intelligence / Profile preview

Histone H4 transcription factor (HINFP)

Target
HINFP
Molecular classification
Transcription factor, Zinc finger protein, Histone gene regulator
01

Overview

The **Histone H4 transcription factor (HINFP)** is a zinc finger transcription factor that binds to conserved DNA motifs adjacent to the TATA box in most histone H4 genes and is critical for the activation of H4 gene expression, especially at the G1/S transition of the cell cycle[1][2][3]. HINFP forms a complex with the coactivator p220^NPAT^ (a substrate of cyclin E/CDK2), serving as the final essential effector in the cyclin E/CDK2/p220^NPAT^/HINFP pathway, which is indispensable for cell proliferation and chromatin assembly following DNA replication[2][3]. The factor is also known as MIZF due to its interaction with methyl-CpG-binding domain proteins such as MBD2, implicating it in DNA methylation and transcriptional repression[1]. HINFP is ubiquitously expressed in proliferating cells and tightly couples histone H4 transcription to cell cycle cues, but is downregulated in post-mitotic cells. Loss of HINFP function in animal models leads to early embryonic lethality due to a failure in cell proliferation and histone H4 gene expression[2][3]. Although its deregulation may contribute to proliferative diseases such as cancer, there are currently no known drugs that directly target HINFP, nor does it serve as a common biomarker or routine therapeutic target[2].

Other names
HINFPHistone nuclear factor PHiNF-PMIZFZNF743MBD2-interacting zinc finger proteinMethyl-CpG-binding protein 2-interacting zinc finger proteinhistone H4 gene-specific protein HiNF-PMBD2-interacting zinc finger 1
02

Biological functions

Regulation of histone H4 gene transcriptionCell cycle progression (G1/S transition control)Chromatin assembly during DNA replicationIntegration of cell cycle signalingInteraction with methylation and transcription repression factors
03

Disease associations

Cancer (deregulation of the cell cycle and histone gene expression)Embryonic lethality if knocked out in mice (developmental defects)
04

Safety considerations

Potential challenges with cell proliferation control if targetedEssential gene (loss-of-function is embryonically lethal in animal models)

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