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Last update 23 Jan 2025

CDC42

Last update 23 Jan 2025

Basic Info

Synonyms

CDC42, CDC42Hs, Cell division control protein 42 homolog

+ [6]

Introduction

Plasma membrane-associated small GTPase which cycles between an active GTP-bound and an inactive GDP-bound state. In active state binds to a variety of effector proteins to regulate cellular responses. Involved in epithelial cell polarization processes. Regulates the bipolar attachment of spindle microtubules to kinetochores before chromosome congression in metaphase (PubMed:15642749). Regulates cell migration (PubMed:17038317). In neurons, plays a role in the extension and maintenance of the formation of filopodia, thin and actin-rich surface projections (PubMed:14978216). Required for DOCK10-mediated spine formation in Purkinje cells and hippocampal neurons. In podocytes, facilitates filopodia and podosomes formation upon DOCK11-activation (PubMed:33523862). Upon activation by CaMKII, modulates dendritic spine structural plasticity by relaying CaMKII transient activation to synapse-specific, long-term signaling (By similarity). Also plays a role in phagocytosis through organization of the F-actin cytoskeleton associated with forming phagocytic cups (PubMed:26465210).

Drugs associated with CDC42

MBQ-167

Target

CDC42

Mechanism

CDC42 inhibitors

Active Org.

University of Puerto Rico-RÃo Piedras [+1]

Originator Org.

University of Puerto Rico-RÃo Piedras

Active Indication

Advanced breast cancer [+1]

Inactive Indication-

Drug Highest PhasePhase 1

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

NCGC00098561

Target

CDC42

Mechanism

CDC42 inhibitors

Active Org.

National Institutes of Health [+1]

Originator Org.

National Institutes of Health [+1]

Active Indication

Breast Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

ARN-24928

Target

CDC42

Mechanism

CDC42 inhibitors

Active Org.

Istituto Italiano di Tecnologia

Originator Org.

University of California

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with CDC42

NCT06075810

/ RecruitingPhase 1

A Phase 1 Open-Label, First-in-Human Trial of Oral MBQ-167 as Single Agent in Participants With Advanced Breast Cancer

A Phase 1, open-label, dose-escalation clinical trial of MBQ-167 in participants with advanced Breast Cancer for whom Standard of Care (SOC) has failed or has proven intolerable.

Start Date09 Nov 2023

Sponsor / Collaborator

MBQ PHARMA INC.Startup

[+1]

100 Clinical Results associated with CDC42

100 Translational Medicine associated with CDC42

0 Patents (Medical) associated with CDC42

7,362

Literatures (Medical) associated with CDC42

31 Dec 2025·Animal Cells and Systems

Loss of neuronal βPix isoforms impairs neuronal morphology in the hippocampus and causes behavioral defects

Article

Author: Park, Dongeun ; Choi, June-Seek ; Lee, Seung Joon ; Shin, Yoon Kyung ; Kwon, Younghee ; Shin, Jung Eun

βPix is a guanine nucleotide exchange factor for the Rac1 and Cdc42 small GTPases, which play important roles in dendritic spine morphogenesis by modulating actin cytoskeleton organization. The formation and plasticity of the dendritic spines are essential for normal brain function. Among the alternatively spliced βPix isoforms, βPix-b and βPix-d are expressed specifically in neurons. Our previous studies using cultured hippocampal neurons identified the roles of βPix-b and βPix-d in spine formation and neurite development, respectively. Here, we analyzed the in vivo role of the neuronal βPix isoforms in brain development and function by using βPix neuronal isoform knockout (βPix-NIKO) mice, in which the expression of the βPix-b and βPix-d isoforms is blocked, while the expression of the ubiquitous βPix-a isoform is maintained. Loss of the neuronal βPix isoforms leads to reduced activity of Rac1 and Cdc42, decreased dendritic complexity and spine density, and increased GluN2B and Ca²⁺/calmodulin-dependent protein kinase IIα expression in the hippocampus. The defects in neurite development, dendritic spine maturation, and synaptic density in cultured βPix-NIKO hippocampal neurons were rescued by the expression of βPix-b or βPix-d. In behavioral studies, βPix-NIKO mice exhibited robust deficits in novel object recognition and decreased anxiety levels. Our findings suggest that neuronal morphogenetic signaling by the neuronal βPix isoforms contributes to normal behaviors.

01 Apr 2025·The Ocular Surface

The role of lysophosphatidic acid and its receptors in corneal nerve regeneration

Article

Author: Bräuer, Anja U ; Brandt, Nicola ; Mertsch, Sonja ; Schrader, Stefan ; Kheyrollah, Maryam

The integrity of corneal nerves is critical for ocular surface health, and damages can lead to Neurotrophic Keratopathy (NK). Despite the regenerative abilities of the peripheral nerve system (PNS), corneal nerve regeneration is often incomplete, and the underlying mechanisms are poorly understood. This study aims to identify potential factors that can enhance corneal nerve regeneration for NK treatment, with a focus on Lysophosphatidic acid (LPA). Thus, the effect of LPA and its underlying pathways in nerve regeneration is investigated in detail using in vitro mouse sensory neurons. To elucidate the impact of LPA as well as to reveal the responsible receptor, several functional assays as well as siRNA-based knock-down experiments were conducted. Additionally, possible changes in underlying pathways were investigated on mRNA levels. LPA-treated neurons significantly reduced fiber growth. However, LPAR2 knockdown neurons (Lpar2-KD) following LPA treatment showed a significant increase in fiber length. Additionally, LPA-treated neurons demonstrated enhanced levels of Lpar2 mRNA. On the other hand, nerve regeneration indicators such as Ngf, Gap-43, and Cdc42, along with LPA downstream signaling components like Pi3k and Ras, were elevated in Lpar2-KD neurons. In conclusion, this study elucidates the inhibitory effects of LPA on fiber outgrowth of sensory neurons. Furthermore, LPAR2 was identified as the responsible receptor for the LPA effect. Thus, Lpar2 knockdown might be a promising therapeutic approach to enhance neuronal regeneration in patients with NK.

01 Mar 2025·Experimental Neurology

Molecular insights into Parkinson's disease and type 2 diabetes mellitus: Metformin's role and genetic pathways explored

Article

Author: Wei, Jianshe ; Wu, Haojie ; Liu, Tingting

Background To explore whether there is a bidirectional relationship between Parkinson's disease (PD) and type 2 diabetes mellitus (T2DM), study the common pathogenic mechanisms, screen relevant genes involved in the pathological process, and predict the potential targets of metformin (Met), so as to develop new therapeutic strategies. Method A two-sample Mendelian randomization (MR) analysis was conducted to analyze the correlation between PD and T2DM. Common confounding genes identified in both PD and T2DM datasets were subjected to GO and KEGG analysis, PPI network analysis, and Hub gene identification. qPCR was used to verify the expression of hub genes in an animal model of T2DM complicated with PD. Subsequently, the analysis focused on whether metformin alleviates the behavioral and pathological manifestations of PD aggravated by T2DM. The intersection of metformin with T2DM and PD targets was identified, and the core targets and signaling pathways were analyzed. Finally, molecular docking analysis was performed between metformin and core proteins to identify the docking sites. Result Through MR analysis, a positive correlation between PD and T2DM was identified, indicating a mutual causal relationship. The hub genes RAC1, TPM2, MGA, and DENND3 are up-regulated in animal models of T2DM with PD. Met targets intersecting with T2DM and PD were analyzed, revealing 17 and 21 intersecting genes respectively, involved in various pathways related to oxidative stress, immune, and inflammation. PPI analysis identified hub genes for T2DM (MMP9, NCF1, CYCS, EIF4E, SOD2) and PD (GFAP, VIM, MOCOS, EIF1, TH, ACTA2, CDC42). Animal models validated the expression of these genes and pathways. Molecular docking analysis explored Met's binding sites on proteins, with lower binding energies indicating greater stability. Conclusion This study contributes to a deeper understanding of the co pathogenesis of PD and T2DM, and provides new insights into the role of metformin in this disease.

News (Medical) associated with CDC42

26 Oct 2022

·www.biospace.com

Kizoo invests in Rejuvenation Startup Mogling Bio

Mogling Bio closes Seed Investment Round with Kizoo Technology Capital BERLIN and ULM, Germany, Oct. 26, 2022 (GLOBE NEWSWIRE) -- Mogling Bio, a privately held biotech company, announces today that it has successfully completed its first seed investment round. Sole investor is venture capital firm Kizoo Technology Capital, a rejuvenation biotech investor focused on startups reversing age-related damage on a cellular and molecular level. Mogling Bio is developing new pharmacological approaches to rejuvenate old stem cells of the hematopoietic (blood cell formation) system. Aging causes stem cells to lose their normal structure by increased activity of the protein CDC42. This loss of structure leads to decreased production and quality of blood and immune cells. It can cause leukemia, various blood diseases, and severely weaken the immune system. Normalizing CDC42 activity can restore structure, order and functionality in those aged stem cells. Treated cells can perform their tasks again in a juvenile way, and thereby contribute to both, the rejuvenation of stem cells and the immune system. The underlying technology was developed over the last 15 years by the two scientific co-founders, Prof. Yi Zheng, co-director of the Cincinnati Children’s Hospital Cancer and Blood Diseases Institute and leader of the Signaling and Drug Discovery Program at the Cincinnati Children’s Research Foundation, and Prof. Dr. Hartmut Geiger, director of the Institute of Molecular Medicine at Ulm University in Germany. “We are really excited that Kizoo's financial support will allow us to pursue our goal of rejuvenating aging stem cells, which are so important for blood cell production and the immune system. Our approach has particular potential in treating diseases of the blood system and improving the immune system”, said Dr. Jürgen Reess, CEO of Mogling Bio. Dr. Reess previously held the position of Senior Vice President at Boehringer Ingelheim Pharma, where he supervised the development, approval, and launch of numerous blockbuster therapies for autoimmune diseases, interstitial lung diseases, central nervous system disorders, and cancer. “We believe that Mogling Bio's technology is groundbreaking by truly rejuvenating old stem cells - not only alleviating age-related diseases, but reversing age-related decline in immune system function”, added Frank Schueler, Managing Director of Kizoo Technology Capital. About Kizoo Kizoo provides seed and follow-on financing with a focus on rejuvenation biotech. Having been entrepreneurs, VC, and mentors in both high-growth tech and biotech companies ourselves for many years with multiple exits and massive value created for the founders, Kizoo now brings this experience to the emerging field of rejuvenation biotech. We see it as a young industry that will eventually outgrow today's largest technology markets. As part of Michael Greve's Forever Healthy Group, Kizoo directly supports the creation of startups turning research on the root causes of aging into therapies and services for human application. Investments include Cellvie, Cyclarity Therapeutics, Revel Pharmaceuticals, Elastrin Therapeutics, LIfT BioSciences and others. For more information, please visit: About Mogling Bio Mogling Bio Inc. is developing new pharmacological approaches to rejuvenate old stem cells of the hematopoietic (blood cell formation) system. Aging causes stem cells to lose their normal structure by increased activity of the protein CDC42. This loss of structure leads to decreased production and quality of blood and immune cells. It can cause leukemia, various blood diseases, and severely weaken the immune system. Normalizing CDC42 activity can restore structure, order and functionality in those aged stem cells. Treated cells can perform their tasks again in a juvenile way, and thereby contribute to both, the rejuvenation of stem cells and the immune system. The underlying technology was developed over the last 15 years by the two scientific co-founders, Prof. Yi Zheng, co-director of the Cincinnati Children’s Hospital Cancer and Blood Diseases Institute and leader of the Signaling and Drug Discovery Program at the Cincinnati Children’s Research Foundation, and Prof. Dr. Hartmut Geiger, director of the Institute of Molecular Medicine at Ulm University in Germany. For more information, please visit: Media Contact for Kizoo: Frank Schueler Managing Director Kizoo Technology Capital fs@kizoo.com Media Contact for Mogling Bio Dr. Jürgen Reess CEO Mogling Bio juergenreess@moglingbio.com

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CDC42

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