Last update 01 Nov 2024

NFYA

Last update 01 Nov 2024

Basic Info

Synonyms

CAAT box DNA-binding protein subunit A, CBF-B, HAP2

+ [4]

Introduction

Component of the sequence-specific heterotrimeric transcription factor (NF-Y) which specifically recognizes a 5'-CCAAT-3' box motif found in the promoters of its target genes. NF-Y can function as both an activator and a repressor, depending on its interacting cofactors. NF-YA positively regulates the transcription of the core clock component BMAL1.

Drugs associated with NFYA

ELB-21

Target

NFYA

Mechanism

NFYA inhibitors

Active Org.-

Originator Org.

ADC Products (UK) Ltd.

Active Indication-

Inactive Indication

Bacterial Infections

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

GWL-78

Target

NFYA

Mechanism

NFYA modulators

Active Org.-

Originator Org.

ADC Products (UK) Ltd.

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with NFYA

100 Translational Medicine associated with NFYA

0 Patents (Medical) associated with NFYA

561

Literatures (Medical) associated with NFYA

01 Nov 2024·Meat Science

Genome to phenome Association for Pork Belly Parameters Elucidates Three Regulation Distinctions: Adipogenesis, muscle formation, and their transcription factors

Article

Author: Kim, Jun-Mo ; Lee, Seung-Hoon

Genome to phenome analysis is necessary in livestock areas because of its various and complex phenotypes. Pork belly is a favorable part of meat worldwide, including East Asia. A previous study has suggested that the three key transcription factors (ZNF444, NFYA and PPARG) affecting pork belly traits include total volume, the volume of total fat and muscle, and component muscles of the corresponding slice. However, other transcription factor genes affecting each slice other than pork belly component traits still needed to be identified. Thus, we aimed to analyze pork belly components at the genome to phenome level for identifying key transcription factor genes and their co-associated networks. The range of node numbers against each component trait via the association weight matrix was from 598 to 3020. Premised on the result, an in silico functional approach was performed. Each co-association network enriched three key transcription factors in adipogenesis and skeletal muscle proliferation, mesoderm development, metabolism, and gene transcription. The three key transcription factors and their related genes may be useful in comprehending their effect of pork belly construction.

01 Oct 2024·Expert review of anticancer therapy

JARID2 activation by NFYA promotes stemness of triple-negative breast cancer cells through the PI3K/AKT pathway.

Article

Author: Wang, Yanfang ; Li, Jianjie ; Liu, Xueliang ; Liu, Yunjiang ; Ma, Xiangmin ; Zhang, Xiangmei

BACKGROUNDThis study aimed to investigate the role of Jumonji AT Rich Interacting Domain 2 (JARID2) in regulating triple-negative breast cancer (TNBC) stemness and its mechanism.RESEARCH DESIGN AND METHODSBioinformatics analysis examined JARID2 expression, prognosis, and transcription factors. Quantitative polymerase chain reaction, western blot, and immunohistochemistry detected expression. Dual luciferase reporter gene and chromatin immunoprecipitation assays verified binding. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and colony formation assay detected viability and proliferation. Sphere formation assay detected the sphere formation efficiency. Flow cytometry detected CD44⁺/CD24^- -marked stem cells. A xenograft tumor model verified the effect of JARID2 in vivo.RESULTSJARID2 and nuclear transcription factor Y subunit α (NFYA) were upregulated in TNBC tissues and positively correlated. Knockdown of JARID2 or NFYA inhibited cell stemness by inhibiting the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB/AKT) signaling pathway. Enforced JARID2 expression rescued the suppressive effect of NFYA knockdown on the PI3K/AKT signaling pathway and cell stemness. Knockdown of JARID2 inhibited tumor growth and cell stemness in mice but was alleviated by concurrent overexpression of NFYA.CONCLUSIONSNFYA promotes TNBC cell stemness by upregulating JARID2 expression and regulating the PI3K/AKT signaling pathway, suggesting JARID2 as a potential target for innovating drugs that target TNBC stem cells.

31 Jul 2024·Cardiovascular Research

Isthmin-1 alleviates cardiac ischaemia/reperfusion injury through cGMP-PKG signalling pathway

Article

Author: Hu, Min ; Wang, Sha-Sha ; Ma, Zhen-Guo ; Tang, Qi-Zhu ; Zeng, Xiao-Feng ; Zhang, Xin ; Hu, Can ; Teng, Teng

AbstractAimsIschaemia/reperfusion (I/R) injury is an important complication of reperfusion therapy for acute myocardial infarction, extremely compromising the cardiac benefits of revascularization; however, specific and efficient treatment for cardiac I/R injury is still lacking. Isthmin-1 (ISM1) is a novel adipokine and plays indispensable roles in regulating glycolipid metabolism and cell survival. The present study aims to investigate the potential role and molecular mechanism of ISM1 in cardiac I/R injury using gain- and loss-of-function approaches.Methods and resultsCardiac-specific ISM1 overexpression and silence were achieved using an adeno-associated virus serotype 9 system, and then these mice were subjected to I/R surgery, followed by biochemical test, echocardiography and histopathologic examinations, etc. Meanwhile, neonatal rat cardiomyocytes (NRCMs) with ISM1 silence or overexpression also received simulated I/R (sI/R) injury to further verify its role in vitro. The potential downstream pathways and molecular targets of ISM1 were screened by RNA sequencing. We also treated injured mice and NRCMs with recombinant ISM1 (rISM1) to explore whether supplementation with ISM1 was sufficient to protect against I/R injury. Furthermore, acute myocardial infarction patients with percutaneous coronary intervention (PCI) and paired healthy controls were included to reveal the clinical relevance of circulating ISM1. Cardiac-specific ISM1 silencing aggravated while ISM1 overexpression alleviated I/R-induced acute cardiac injury and cardiac remodelling and dysfunction. Mechanistically, ISM1 targeted αvβ5 integrin to facilitate the nuclear accumulation of nuclear transcription factor Y subunit alpha, transcriptionally increased soluble guanylyl cyclase beta subunit expression, and eventually enhanced cGMP generation. Besides, we confirmed that treatment with rISM1 before or after reperfusion could confer cardioprotective effects in mice. Clinically, lower ISM1 levels post-PCI was associated with worse outcome in patients.ConclusionISM1 can protect against cardiac I/R injury through cGMP-PKG signalling pathway, and it is a promising therapeutic and predictive target of cardiac I/R injury.

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