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Last update 08 May 2025

GLI2 x GLI1

Last update 08 May 2025

Basic Info

Related Targets

GLI2GLI1

Drugs associated with GLI2 x GLI1

JC19

Target

GLI1 x GLI2

Mechanism

GLI1 inhibitors [+1]

Active Org.

Alfasigma SpA

Originator Org.

Alfasigma SpA

Active Indication

Melanoma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

GANT61

Target

GLI1 x GLI2

Mechanism

GLI1 inhibitors [+1]

Active Org.

Health Sciences University of Hokkaido

Originator Org.

Health Sciences University of Hokkaido

Active Indication

Melanoma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with GLI2 x GLI1

100 Translational Medicine associated with GLI2 x GLI1

0 Patents (Medical) associated with GLI2 x GLI1

697

Literatures (Medical) associated with GLI2 x GLI1

01 Jun 2025·Current Pharmaceutical Design

Identification of Ferroptosis-related Genes for Diabetic Nephropathy by Bioinformatics and Experimental Validation

Article

Author: Yu, Jiangyi ; Song, Siyuan

Objective:The present study delves into the exploration of diagnostic biomarkers linked with ferroptosis in the context of diabetic nephropathy, unraveling their underlying molecular mechanismsMethods:In this study, we retrieved datasets GSE96804 and GSE30529 as the training cohort, followed by screening for Differentially Expressed Genes (DEGs). By intersecting these DEGs with known ferroptosisrelated genes, we obtained the differentially expressed genes related to ferroptosis (DEFGs). Subsequently, Weighted Correlation Network Analysis (WGCNA) was carried out to identify key modules associated with Diabetic Nephropathy (DN), culminating in the identification of a significant gene. Enrichment analysis and Gene Set Enrichment Analysis (GSEA) were then carried out on the DEFGs and genes linked to the significant gene. To validate our findings, we employed cohorts GSE30528 and GSE43950, utilizing ROC curve analysis to assess diagnostic efficacy for DN, as measured by the area under the curve (AUC). Immune cell infiltration was analyzed and compared between groups using the CIBERSORT algorithm. Bayesian colocalization analysis was performed to examine the co-location of DEFGs and DN. Finally, to validate the hub genes identified, we conducted quantitative real-time polymerase chain reaction (qRT-PCR) experiments in vitro.Results:FUZ, GLI1, GLI2, GLI3, and DVL2 were identified as the hub genes. Functional enrichment analysis demonstrated that ferroptosis and immune response play an important role in DN. ROC analysis showed that the identified genes had good diagnostic efficiency in DN. The results of the immune infiltration analysis showed that there may be crosstalk between ferroptosis and immune cells in DN. Bayesian co-localization analysis revealed the genetic correlation between the hub genes and DN. The outcomes of the qRT-PCR analyses corroborated the reliability of the identified hub genes as robust molecular markers for targeted therapy in DN.Conclusion:The interplay between immune inflammatory reactions and ferroptosis emerges as a crucial pathogenic mechanism, offering novel insights into the molecular therapy of DN. Furthermore, the identification of FUZ, GLI1, GLI2, GLI3, and DVL2 as potential targets holds promise for future therapeutic interventions aimed at treating DN.

01 May 2025·Genes & Diseases

Sonic Hedgehog potentiates BMP9-induced osteogenic differentiation of mesenchymal stem cells

Article

Author: Zhang, Lulu ; Luo, Jinyong ; Jiwa, Habu ; Ji, Caixia ; Xie, Zhou ; Luo, Xiaoji ; Li, Ziyun

Bone morphogenetic protein 9 (BMP9) has remarkable potential to induce the differentiation of mesenchymal stem cells (MSCs) towards the osteoblastic lineage. Additionally, research suggests that certain growth factors have the ability to potentiate BMP9-induced osteogenic differentiation of MSCs. Sonic Hedgehog (Shh) plays an indispensable role in the regulation of skeletal development. The objective of this research was to assess the potential influence of Shh on BMP9-induced osteogenic differentiation of MSCs. Our findings indicated that Shh effectively enhanced BMP9-induced early and late osteogenic differentiation of MSCs, and increased BMP9-induced expression/transcriptional activity of osteogenesis-related transcription factors. Besides, it was observed that Shh promoted BMP9-induced ectopic bone formation of MSCs in vivo. Moreover, BMP9 was able to facilitate the repair of bone defects in rats, while Shh further accelerated this reparative process. Mechanistically, Shh enhanced the activation of the Smad1/5/8 signaling pathway which was induced by BMP9. Furthermore, GANT-61, an inhibitor of Gli1 and Gli2, attenuated the enhancing effect of Shh on BMP9-induced osteogenic differentiation of MSCs. Collectively, the co-administration of BMP9 and Shh may present a promising therapeutic approach for the treatment of fracture nonunion, delayed fracture healing, and bone defects.

14 Mar 2025·Science Advances

Collaborative role of two distinct cilium-specific cytoskeletal systems in driving Hedgehog-responsive transcription factor trafficking

Article

Author: Chadha, Abhishek ; Ku, Pei-I ; Williams, David S. ; Engelke, Martin F. ; Sreeja, Jamuna S. ; Subramanian, Radhika

In vertebrate Hedgehog (Hh) signaling, the precise output of the final effectors, GLI (glioma-associated oncogene) transcription factors, depends on the primary cilium. Upon pathway initiation, generating the precise levels of the activator form of GLI depends on its concentration at the cilium tip. The mechanisms underlying this critical step in Hh signaling are unclear. We developed an assay to visualize GLI2, the primary GLI activator isoform, at single-particle resolution within the cilium. We found that GLI2 is a cargo of intraflagellar transport (IFT) machinery. Anterograde-biased IFT loading of GLI2 in a restricted time window following pathway activation results in the tip accumulation of GLI2. Unexpectedly, we found that the conserved Hh regulator KIF7, a nonmotile kinesin, is important for the temporal control of IFT-mediated GLI2 transport and retention of GLI2 at the cilium tip. Our findings underscore a design principle where a cilia-specific cytoskeletal transport system and an Hh pathway–specific cytoskeletal protein collaboratively regulate GLI2 trafficking for Hh signaling.

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