HINFP

Last update 08 May 2025

Basic Info

Synonyms

DKFZP434F162, HiNF-P, HINFP

+ [6]

Introduction

Transcriptional repressor that binds to the consensus sequence 5'-CGGACGTT-3' and to the RB1 promoter. Transcriptional activator that promotes histone H4 gene transcription at the G1/S phase transition in conjunction with NPAT. Also activates transcription of the ATM and PRKDC genes. Autoregulates its expression by associating with its own promoter.

100 Clinical Results associated with HINFP

100 Translational Medicine associated with HINFP

0 Patents (Medical) associated with HINFP

Literatures (Medical) associated with HINFP

01 May 2024·Aging Cell

Histone deficiency and hypoacetylation in the aging retinal pigment epithelium

Article

Author: Prajapati, Subhash C ; Mohan, Kabhilan ; Jung, Kyungsik ; Dubey, Sushil K ; Liu, Xinan ; Kleinman, Mark E ; Tian, Wenjian ; Roney, Jacob ; Dubey, Rashmi ; Abney, Jennifer ; Hernandez, Alvaro G ; Liu, Jinze ; Giarmarco, Michelle M

AbstractHistones serve as a major carrier of epigenetic information in the form of post‐translational modifications which are vital for controlling gene expression, maintaining cell identity, and ensuring proper cellular function. Loss of histones in the aging genome can drastically impact the epigenetic landscape of the cell leading to altered chromatin structure and changes in gene expression profiles. In this study, we investigated the impact of age‐related changes on histone levels and histone acetylation in the retinal pigment epithelium (RPE) and retina of mice. We observed a global reduction of histones H1, H2A, H2B, H3, and H4 in aged RPE/choroid but not in the neural retina. Transcriptomic analyses revealed significant downregulation of histones in aged RPE/choroid including crucial elements of the histone locus body (HLB) complex involved in histone pre‐mRNA processing. Knockdown of HINFP, a key HLB component, in human RPE cells induced histone loss, senescence, and the upregulation of senescence‐associated secretory phenotype (SASP) markers. Replicative senescence and chronological aging in human RPE cells similarly resulted in progressive histone loss and acquisition of the SASP. Immunostaining of human retina sections revealed histone loss in RPE with age. Acetyl‐histone profiling in aged mouse RPE/choroid revealed a specific molecular signature with loss of global acetyl‐histone levels, including H3K14ac, H3K56ac, and H4K16ac marks. These findings strongly demonstrate histone loss as a unique feature of RPE aging and provide critical insights into the potential mechanisms linking histone dynamics, cellular senescence, and aging.

01 Apr 2024·BMJ Neurology Open

Shared genetic aetiology of Alzheimer’s disease and age-related macular degeneration by APOC1 and APOE genes

Article

Author: Liu, Shunming ; Kiburg, Katerina ; Zhang, Xueli ; Zhu, Zhuoting ; Wang, Wei ; Huang, Yu ; Zhang, Lei ; O'Brien, Terence J ; Yu, Honghua ; Zhang, Xiayin ; Bao, Yining ; Wang, Jing ; Shang, Xianwen ; Ha, Jason ; He, Mingguang ; Kwan, Patrick

BackgroundAlzheimer’s disease (AD) and age-related macular degeneration (AMD) share similar pathological features, suggesting common genetic aetiologies between the two. Investigating gene associations between AD and AMD may provide useful insights into the underlying pathogenesis and inform integrated prevention and treatment for both diseases.MethodsA stratified quantile–quantile (QQ) plot was constructed to detect the pleiotropy among AD and AMD based on genome-wide association studies data from 17 008 patients with AD and 30 178 patients with AMD. A Bayesian conditional false discovery rate-based (cFDR) method was used to identify pleiotropic genes. UK Biobank was used to verify the pleiotropy analysis. Biological network and enrichment analysis were conducted to explain the biological reason for pleiotropy phenomena. A diagnostic test based on gene expression data was used to predict biomarkers for AD and AMD based on pleiotropic genes and their regulators.ResultsSignificant pleiotropy was found between AD and AMD (significant leftward shift on QQ plots). APOC1 and APOE were identified as pleiotropic genes for AD–AMD (cFDR <0.01). Network analysis revealed that APOC1 and APOE occupied borderline positions on the gene co-expression networks. Both APOC1 and APOE genes were enriched on the herpes simplex virus 1 infection pathway. Further, machine learning-based diagnostic tests identified that APOC1, APOE (areas under the curve (AUCs) >0.65) and their upstream regulators, especially ZNF131, ADNP2 and HINFP, could be potential biomarkers for both AD and AMD (AUCs >0.8).ConclusionIn this study, we confirmed the genetic pleiotropy between AD and AMD and identified APOC1 and APOE as pleiotropic genes. Further, the integration of multiomics data identified ZNF131, ADNP2 and HINFP as novel diagnostic biomarkers for AD and AMD.

01 Jul 2023·Gene

Spatiotemporal higher-order chromatin landscape of human histone gene clusters at histone locus bodies during the cell cycle in breast cancer progression

Article

Author: Gao, Cong ; Boyd, Joseph R. ; Kabala, Fleur ; Stein, Janet L. ; Fritz, Andrew J. ; van Wijnen, Andre J. ; Seward, David J. ; Bright, Kathleen ; Pegoraro, Gianluca ; Lian, Jane B. ; Misteli, Tom ; Stein, Gary S. ; Ghule, Prachi N. ; Macfarlane, Jill ; Frietze, Seth ; Bouffard, Nicole A.

Human Histone Locus Bodies (HLBs) are nuclear subdomains comprised of clustered histone genes that are coordinately regulated throughout the cell cycle. We addressed temporal-spatial higher-order genome organization for time-dependent chromatin remodeling at HLBs that supports control of cell proliferation. Proximity distances of specific genomic contacts within histone gene clusters exhibit subtle changes during the G1 phase in MCF10 breast cancer progression model cell lines. This approach directly demonstrates that the two principal histone gene regulatory proteins, HINFP (H4 gene regulator) and NPAT, localize at chromatin loop anchor-points, denoted by CTCF binding, supporting the stringent requirement for histone biosynthesis to package newly replicated DNA as chromatin. We identified a novel enhancer region located ∼ 2 MB distal to histone gene sub-clusters on chromosome 6 that consistently makes genomic contacts with HLB chromatin and is bound by NPAT. During G1 progression the first DNA loops form between one of three histone gene sub-clusters bound by HINFP and the distal enhancer region. Our findings are consistent with a model that the HINFP/NPAT complex controls the formation and dynamic remodeling of higher-order genomic organization of histone gene clusters at HLBs in early to late G1 phase to support transcription of histone mRNAs in S phase.

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HINFP

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