FOXB1

Last update 08 May 2025

Basic Info

Synonyms

FKH5, forkhead box B1, Forkhead box protein B1

+ [3]

Introduction

Transcription factor expressed by neural progenitor cells in specific regions of the embryonic neuroepithelium. Essential for the mammillary nuclei maintenance. Negatively regulates the proliferation of oligodendrocyte progenitors and promotes oligodendrocyte maturation. Also expressed in mammary glands, plays a role in lactation, controls development of mammary glands and the inferior colliculi of the midbrain in the central nervous system that regulates the milk-ejection reflex.

100 Clinical Results associated with FOXB1

100 Translational Medicine associated with FOXB1

0 Patents (Medical) associated with FOXB1

Literatures (Medical) associated with FOXB1

01 Feb 2025·Biogerontology

Forkhead box P1 transcriptionally activates IGF-1 to lighten ox-LDL-induced endothelial cellular senescence by inactivating NLRP3 inflammasome

Article

Author: Deng, Siqi ; Lao, Meili ; Hao, Jingwen ; Zheng, Huihui

Endothelial cell (EC) senescence is a major contributor in atherosclerosis (AS) development. Herein, the role of forkhead box P transcription factor 1 (FOXP1) and insulin-like growth factor (IGF)-1 in regulating EC senescence during AS progression was investigated. The mRNA and protein expressions were assessed using qRT-PCR and western blot. IL-1β and IL-18 secretion levels were analyzed by ELISA. Cell viability and pyroptosis were determined by MTT assay and flow cytometry, respectively. SA β-Gal staining was used to measure cell senescence. Tube formation assay was adopted to detect the angiogenesis ability. Dual-luciferase reporter and ChIP assays were used to investigate the relationship between FOXP1 and IGF‑1. ox-LDL stimulation significantly reduced FOXP1 and IGF-1 expression levels in human aortic endothelial cells (HAECs). FOXP1 or IGF-1 overexpression both mitigated ox-LDL-induced cellular senescence and NLRP3 activation in HAECs. It was subsequently revealed that FOXB1 transcriptionally activated IGF-1 expression in HAECs by binding to IGF-1 promoter. Rescue experiments demonstrated that IGF-1 silencing abolished the inhibitory impact of FOXP1 overexpression on ox-LDL-induced cellular senescence and NLRP3 activation in HAECs. FOXP1 transcriptionally activated IGF-1 to lighten ox-LDL-induced endothelial cellular senescence by inactivating NLRP3 inflammasome.

01 Jan 2025·Cell Reports

Dual-nuclease single-cell lineage tracing by Cas9 and Cas12a

Article

Author: Zhu, Miao ; Yu, Xinran ; Wang, Li ; Li, Meishi ; Liao, Yuanxin ; Chen, Cheng ; Peng, Guangdun

Single-cell lineage tracing based on CRISPR-Cas9 gene editing enables the simultaneous linkage of cell states and lineage history at a high resolution. Despite its immense potential in resolving the cell fate determination and genealogy within an organism, existing implementations of this technology suffer from limitations in recording capabilities and considerable barcode dropout. Here, we introduce DuTracer, a versatile tool that utilizes two orthogonal gene editing systems to record cell lineage history at single-cell resolution in an inducible manner. DuTracer shows the ability to enhance lineage recording with minimized target dropouts and potentially deeper tree depths. Applying DuTracer in mouse embryoid bodies and neuromesodermal organoids illustrates the lineage relationship of different cell types and proposes potential lineage-biased molecular drivers, showcased by identifying transcription factor Foxb1 as a modulator in the cell fate determination of neuromesodermal progenitors. Collectively, DuTracer facilitates the precise and regulatory interrogation of cellular lineages of complex biological processes.

25 Feb 2022·Science AdvancesQ1 · CROSS-FIELD

A circuit from dorsal hippocampal CA3 to parvafox nucleus mediates chronic social defeat stress–induced deficits in preference for social novelty

Q1 · CROSS-FIELD

ArticleOA

Author: Wang, Fang ; Li, Liang-Xia ; Chen, Jian-Guo ; Deng, Si-Long ; Lv, Qiu ; Wang, Zhong-Yuan ; Zhou, Zi-Xiang ; Liu, Yang

The preference for social novelty is crucial to the social life of humans and rodents. However, the neural mechanisms underlying social novelty preference are poorly understood. Here, we found that chronic social defeat stress (CSDS) reduced the preference for social novelty in mice by impairing the response of CaMKIIα + neurons in the CA3 region of dorsal hippocampus (dCA3) during approach to an unfamiliar mouse. The deficits of social novelty preference in CSDS-treated mice were reversed by activating the output from dCA3 to the GABAergic neurons in the lateral septum (LS). The activation of GABAergic projection from LS recruited a circuit that inhibited the Foxb1 + neurons in the parvafox nucleus (PFN), which drove social avoidance by projecting to the lateral periaqueductal gray (lPAG). These results suggest that a previously unidentified circuit of dCA3 CaMKIIα+ →LS GABA+ →PFN Foxb1+ →lPAG mediates the deficits of social novelty preference induced by CSDS.

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FOXB1

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