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Last update 08 May 2025

DLX2

Last update 08 May 2025

Basic Info

Synonyms

distal-less homeobox 2, DLX2, Homeobox protein DLX-2

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Introduction

Acts as a transcriptional activator (By similarity). Activates transcription of CGA/alpha-GSU, via binding to the downstream activin regulatory element (DARE) in the gene promoter (By similarity). Plays a role in terminal differentiation of interneurons, such as amacrine and bipolar cells in the developing retina. Likely to play a regulatory role in the development of the ventral forebrain (By similarity). May play a role in craniofacial patterning and morphogenesis (By similarity).

Drugs associated with DLX2

CN116970571

Patent Mining

Target

DLX2

Mechanism-

Active Org.

Sichuan University

Originator Org.

Sichuan University

Active Indication

Neurologic Manifestations

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with DLX2

100 Translational Medicine associated with DLX2

0 Patents (Medical) associated with DLX2

435

Literatures (Medical) associated with DLX2

01 Jun 2025·Neural Regeneration Research

Characteristic changes in astrocyte properties during astrocyte-to-neuron conversion induced by NeuroD1/Ascl1/Dlx2

Article

Author: Wang, Yuchen ; He, Qing ; Chen, Gong ; Zhang, Kanghong ; Xu, Yuge ; Zhu, Mengjie ; Liang, Zhile ; Wang, Zhen

JOURNAL/nrgr/04.03/01300535-202506000-00030/figure1/v/2024-08-08T040853Z/r/image-tiff Direct in vivo conversion of astrocytes into functional new neurons induced by neural transcription factors has been recognized as a potential new therapeutic intervention for neural injury and degenerative disorders. However, a few recent studies have claimed that neural transcription factors cannot convert astrocytes into neurons, attributing the converted neurons to pre-existing neurons mis-expressing transgenes. In this study, we overexpressed three distinct neural transcription factors––NeuroD1, Ascl1, and Dlx2––in reactive astrocytes in mouse cortices subjected to stab injury, resulting in a series of significant changes in astrocyte properties. Initially, the three neural transcription factors were exclusively expressed in the nuclei of astrocytes. Over time, however, these astrocytes gradually adopted neuronal morphology, and the neural transcription factors was gradually observed in the nuclei of neuron-like cells instead of astrocytes. Furthermore, we noted that transcription factor-infected astrocytes showed a progressive decrease in the expression of astrocytic markers AQP4 (astrocyte endfeet signal), CX43 (gap junction signal), and S100β. Importantly, none of these changes could be attributed to transgene leakage into pre-existing neurons. Therefore, our findings suggest that neural transcription factors such as NeuroD1, Ascl1, and Dlx2 can effectively convert reactive astrocytes into neurons in the adult mammalian brain.

01 May 2025·Glia

Single‐Cell RNA Sequencing Uncovers Molecular Features Underlying the Disrupted Neurogenesis Following Traumatic Brain Injury

Article

Author: Liu, Cong ; He, Xuan‐Cheng ; Shao, Fang‐Hong ; Zhou, Bing ; Du, Hong‐Zhen ; Liu, Chang‐Mei ; Teng, Zhao‐Qian

ABSTRACTTraumatic brain injury (TBI) is a leading cause of death and disability worldwide, with limited effective treatment strategies. Endogenous neural stem cells (NSCs) give rise to neurons and glial cells throughout life. However, NSCs are more likely to differentiate into glial cells rather than neurons at the lesion site after TBI and the underlying molecular mechanism remains largely unknown. Here, we performed large‐scale single‐cell transcriptome sequencing of subventricular zone (SVZ) NSCs and NSCs‐derived cells in the mouse brain, and provide molecular evidence for previous observations that glial differentiation of NSCs prevails after TBI. In addition, we show that the disrupted neurogenesis following TBI is caused by the reduction of a NSC subcluster (NSC‐4) expressing the neuronal gene Tubb3. Finally, we demonstrate that the transcriptional factor Dlx2 is significantly downregulated in NSC‐4, and Dlx2 overexpression is sufficient to drive NSCs towards neuronal lineage differentiation at the expense of astrocytic lineage differentiation under pro‐inflammatory conditions.

01 Apr 2025·Stem Cell Reviews and Reports

Identification of Cell Fate Determining Transcription Factors for Generating Brain Endothelial Cells

Article

Author: De Smedt, Jonathan ; Verfaillie, Catherine ; Balaton, Bradley ; Ramezankhani, Roya ; Vanmarcke, Gert ; Vosough, Massoud ; Toprakhisar, Burak ; van der Veer, Bernard K ; Chai, Yoke Chin ; van Grunsven, Leo ; Tricot, Tine

AbstractReliable models of the blood-brain barrier (BBB), wherein brain microvascular endothelial cells (BMECs) play a key role in maintenance of barrier function, are essential tools for developing therapeutics and disease modeling. Recent studies explored generating BMEC-like cells from human pluripotent stem cells (hPSCs) by mimicking brain-microenvironment signals or genetic reprogramming. However, due to the lack of comprehensive transcriptional studies, the exact cellular identity of most of these cells remains poorly defined. In this study we aimed to identify the most likely master transcription factors (TFs) for inducing brain endothelial cell (EC) fate and assess the transcriptomic changes following their introduction into immature ECs. Therefore, we first generated PSC-derived immature ECs by transient overexpression of the TF, ETV2. Subsequently, by performing an extensive meta-analysis of transcriptome studies of brain and non-brain ECs, 12 candidate TFs were identified, which might fate immature ECs towards cells with brain EC features. Following combinatorial overexpression of these 12 TFs tagged with unique barcodes, single cell transcriptomics identified a subset of transduced cells that resembled mid-gestational human brain ECs. Assessment of the TF barcodes present in these cells revealed significant enrichment of the TFs ZIC3, TFAP2C, TFAP2A, and DLX2. These TFs might be useful to fate PSC-EC to BMEC-like cells, which could be incorporated in human in vitro BBB models.Graphical Abstract

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DLX2

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