Last update 01 Nov 2024

DLX2

Last update 01 Nov 2024

Basic Info

Synonyms

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

+ [1]

Introduction

Acts as a transcriptional activator. 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. May play a role in craniofacial patterning and morphogenesis.

Drugs associated with DLX2

WO2022072310

Patent Mining

Target

DLX2

Mechanism-

Active Org.

NeuExCell Therapeutics, Inc.Startup

Originator Org.

NeuExCell Therapeutics, Inc.Startup

Active Indication

Infectious Diseases [+1]

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

424

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 ; Zhu, Mengjie ; Xu, Yuge ; Zhang, Kanghong ; 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.

31 Dec 2024·Autoimmunity

Osteocyte-derived exosomes regulate the DLX2/wnt pathway to alleviate osteoarthritis by mediating cartilage repair

Article

Author: Zhang, Yuanyuan ; Pan, Liyan ; Li, Lijuan ; Li, Wei ; Lu, Li ; Zhi, Shenshen ; Xu, Wenjuan

BACKGROUNDChondrocyte viability, apoptosis, and migration are closely related to cartilage injury in osteoarthritis (OA) joints. Exosomes are identified as potential therapeutic agents for OA.OBJECTIVEThis study aimed to investigate the role of exosomes derived from osteocytes in OA, particularly focusing on their effects on cartilage repair and molecular mechanisms.METHODSAn injury cell model was established by treating chondrocytes with IL-1β. Cartilage repair was evaluated using cell counting kit-8, flow cytometry, scratch test, and Western Blot. Molecular mechanisms were analyzed using quantitative real-time PCR, bioinformatic analysis, and Western Blot. An OA mouse model was established to explore the role of exosomal DLX2 in vivo.RESULTSOsteocyte-released exosomes promoted cell viability and migration, and inhibited apoptosis and extracellular matrix (ECM) deposition. Moreover, exosomes upregulated DLX2 expression, and knockdown of DLX2 activated the Wnt pathway. Additionally, exosomes attenuated OA in mice by transmitting DLX2.CONCLUSIONOsteocyte-derived exosomal DLX2 alleviated IL-1β-induced cartilage repair and inactivated the Wnt pathway, thereby alleviating OA progression. The findings suggested that osteocyte-derived exosomes may hold promise as a treatment for OA.

01 Oct 2024·Developmental Neurobiology

Efficient Dlx2‐mediated astrocyte‐to‐neuron conversion and inhibition of neuroinflammation by NeuroD1

Article

Author: Bai, Xiao‐Ni ; Wang, Tao ; Chen, Gong ; Xu, Yu‐Ge ; Xiang, Zong‐Qin ; Xu, Liang ; Lin, Jian‐Hua ; Liu, Min‐Hui

AbstractIn vivo astrocyte‐to‐neuron (AtN) conversion induced by overexpression of neural transcriptional factors has great potential for neural regeneration and repair. Here, we demonstrate that a single neural transcriptional factor, Dlx2, converts mouse striatal astrocytes into neurons in a dose‐dependent manner. Lineage‐tracing studies in Aldh1l1‐CreERT2 mice confirm that Dlx2 can convert striatal astrocytes into DARPP32+ and Ctip2+ medium spiny neurons (MSNs). Time‐course studies reveal a gradual conversion from astrocytes to neurons in 1 month, with a distinct intermediate state in between astrocytes and neurons. Interestingly, when Dlx2‐infected astrocytes start to lose astrocytic markers, the other local astrocytes proliferate to maintain astrocytic levels in the converted areas. Unexpectedly, although Dlx2 efficiently reprograms astrocytes into neurons in the gray matter striatum, it also induces partial reprogramming of astrocytes in the white matter corpus callosum. Such partial reprogramming of white matter astrocytes is associated with neuroinflammation, which can be suppressed by the addition of NeuroD1. Our results highlight the importance of investigating AtN conversion in both the gray matter and white matter to thoroughly evaluate therapeutic potentials. This study also unveils the critical role of anti‐inflammation by NeuroD1 during AtN conversion.

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DLX2

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