ZNF431

Last update 08 May 2025

Basic Info

Synonyms

KIAA1969, zinc finger protein 431, ZNF431

Introduction

Sequence-specific DNA binding transcriptional repressor. Represses target gene transcription by recruiting HDAC1 and HDAC2 histone deacetylases. Acts as a specific transcriptional repressor for PTCH1 during embryonic development. Required for osteoblast differentiation and sonic hedgehog/SHH signaling response. Binds to the consensus site 5'-GCGCCC-3' in the promoter of PTCH1 (By similarity).

100 Clinical Results associated with ZNF431

100 Translational Medicine associated with ZNF431

0 Patents (Medical) associated with ZNF431

Literatures (Medical) associated with ZNF431

01 Mar 2025·Health Science Reports

Hyper IgE Syndromes: Understanding, Management, and Future Perspectives: A Narrative Review

Article

Author: Tafrishi, Rana ; Pasdar, Alireza ; Karimiani, Ehsan Ghayoor ; Safi, Mojtaba ; Salehi, Mohammad ; Neshati, Zeinab ; Ahanchian, Hamid

ABSTRACTBackground and AimHyper IgE syndromes (HIES) are rare primary immunodeficiency characterized by susceptibility to specific infections, eczema, and elevated IgE levels. Pathogenic mutations in STAT3, IL6R, IL6ST, ERBB2IP, PGM3, ZNF431, SPINK5, TGFBR1/2, and CARD11 have been identified as genetic factors contributing to phenotypes of HIES lead to hindered differentiation and activity, aberrant signaling cascades and disrupting immune regulation. HIES present a diverse clinical symptoms, challenging diagnosis and management; understanding its pathophysiology, genetics, and immunological abnormalities offer hope for improved outcomes. In this review we aim to provide a comprehensive understanding of the condition and also discuss latest updates on pathological features, clinical spectrum and its variability, immunological abnormalities, inheritance patterns, new candidate genes, challenges, management strategies, epidemiology and future directions of HIES.MethodsThis review conducted an extensive search of information from multiple databases, including PubMed, Scopus, WHO, and ClinVar to ensure comprehensive coverage. Preference was given to articles published recently to capture the latest research and developments. Endnote was employed as a reference manager. The relevant literature was meticulously reviewed to address the objectives of the study.ResultsMissense, nonsense, and frameshift variants are commonly observed in HIES. Understanding these genetic mutations is key to diagnosing and managing conditions such as Hyper‐IgE recurrent infection syndromes (linked to IL6R, STAT3, and ZNF341 mutations), Atopy associated with ERBIN mutations which links STAT3 and TGF‐β pathway, Immunodeficiency 23 (caused by PGM3 mutations), Netherton syndrome (resulting from SPINK5 mutations), and Loeys‐Dietz syndrome (related to TGFBR mutations). Each year, new genes and variants responsible for this type of immune deficiency are added to the list.ConclusionAlthough rare, HIES significantly impacts patients due to its complex medical manifestations and need for lifelong management. Identifying casual variants is essential for effective clinical management of these complex conditions.

01 Apr 2024·Cellular Oncology

Plasma cell signatures predict prognosis and treatment efficacy for lung adenocarcinoma

Article

Author: Tao, Yongguang ; Liu, Shuang ; Tang, Jun ; Shu, Long

PURPOSEThis study aims to identify key genes regulating tumor infiltrating plasma cells (PC) and provide new insights for innovative immunotherapy.METHODSKey genes related to PC were identified using machine learning in lung adenocarcinoma (LUAD) patients. A prognostic model called PC scores was developed using TCGA data and validated with GEO cohorts. We assessed the molecular background, immune features, and drug sensitivity of the high PC scores group. Real-time PCR was utilized to assess the expression of hub genes in both localized LUAD patients and LUAD cell lines.RESULTSWe constructed PC scores based on seventeen PC-related hub genes (ELOVL6, MFI2, FURIN, DOK1, ERO1LB, CLEC7A, ZNF431, KIAA1324, NUCB2, TXNDC11, ICAM3, CR2, CLIC6, CARNS1, P2RY13, KLF15, and SLC24A4). Higher age, TNM stage, and PC scores independently predicted shorter overall survival. The AUC value of PC scores for one year, three years, and five years of overall survival were 0.713, 0.716, and 0.690, separately. The nomogram model that integrated age, stage, and PC scores showed significantly higher predictive value than stage alone (P < 0.01). High PC scores group exhibited an immune suppressing microenvironment with lower B, CD8 + T, CD4 + T, and dendritic cell infiltration. Docetaxel, gefitinib, and erlotinib had lower IC50 in high PC groups (P < 0.001). After validation through the local cohort and in vitro experiments, we ultimately confirmed three key potential targets: MFI2, KLF15, and CLEC7A.CONCLUSIONWe proposed a prediction mode which can effectively identify high-risk LUAD patients and found three novel genes closely correlated with PC tumor infiltration.

01 Apr 2019·Immunology & Cell Biology

Hyper IgE syndromes: clinical and molecular characteristics

Review

Author: Ochs, Hans D ; Al‐Shaikhly, Taha

AbstractHyper IgE syndromes comprise a group of rare primary immunodeficiency disorders characterized by a triad of atopic dermatitis, recurrent skin and lung infections along with elevated IgE levels. Job syndrome or autosomal dominant hyper IgE syndrome because of heterozygous loss‐of‐function mutations with dominant negative effect in signal transducer and activator of transcription‐3 is the prototype of these disorders. However, several other genetically characterized immunodeficiency disorders have been identified over the past decade and joined the umbrella of hyper IgE syndromes including autosomal recessive mutations in the DOCK8,ZNF431 and PGM3 genes and heterozygous mutations with dominant negative effect in the CARD11 gene. Moreover, a number of phenotypically distinct immunodeficiency disorders can mimic hyper IgE syndromes, adding to the diagnostic challenge. Herein, we will concisely review these disorders, their molecular bases, highlighting key distinguishing clinical and laboratory findings and therapeutic options.

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ZNF431

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