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Last update 23 Jan 2025

GNA13

Last update 23 Jan 2025

Basic Info

Synonyms

G alpha-13, G protein subunit alpha 13, G-protein subunit alpha-13

+ [4]

Introduction

Guanine nucleotide-binding proteins (G proteins) are involved as modulators or transducers in various transmembrane signaling systems (PubMed:15240885, PubMed:16787920, PubMed:16705036, PubMed:27084452). Activates effector molecule RhoA by binding and activating RhoGEFs (ARHGEF1/p115RhoGEF, ARHGEF11/PDZ-RhoGEF and ARHGEF12/LARG) (PubMed:15240885, PubMed:12515866). GNA13-dependent Rho signaling subsequently regulates transcription factor AP-1 (activating protein-1) (By similarity). Promotes tumor cell invasion and metastasis by activating RhoA/ROCK signaling pathway (PubMed:16787920, PubMed:16705036, PubMed:27084452). Inhibits CDH1-mediated cell adhesion in process independent from Rho activation (PubMed:11976333).

Drugs associated with GNA13

M-3mP6

Target

GNA13

Mechanism

GNA13 inhibitors

Active Org.

University of Illinois

Originator Org.

University of Illinois

Active Indication

Myocardial Ischemia [+2]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with GNA13

100 Translational Medicine associated with GNA13

0 Patents (Medical) associated with GNA13

185

Literatures (Medical) associated with GNA13

01 Jan 2025·American Journal of Hematology

High‐grade B‐cell lymphoma not otherwise specified, with diffuse large B‐cell lymphoma gene expression signatures: Genomic analysis and potential therapeutics

Article

Author: Heavican‐Foral, Tayla B. ; Zhang, Xuan ; Yu, Jiayu ; Fu, Kai ; Herek, Tyler A. ; Issa, Issa Ismail ; Bhagavathi, Sharath Kumar ; Lone, Waseem ; Mir, Abdul Rouf ; McKeithan, Timothy W. ; Song, Joo ; Green, Michael ; Xu, Alexander M. ; Saumyaranjan, Mallick ; Jochum, Dylan ; Dave, Bhavana J. ; Bi, Chengfeng ; Iqbal, Javeed ; Weisenburger, Dennis D. ; Alkhinji, Aisha Ahmad ; Sharma, Sunandini ; Merchant, Akil ; Greiner, Timothy C. ; Vose, Julie ; El‐Gamal, Dalia ; Amador, Catalina ; Bouska, Alyssa ; Hartert, Keenan ; Shah, Ab Rauf ; Chan, Wing C.

AbstractHigh‐grade B‐cell lymphoma not otherwise specified (HGBCL, NOS) has overlapping morphological and genetic features with diffuse large B‐cell lymphoma (DLBCL) and Burkitt lymphoma (BL), leading to uncertainty in its diagnosis and clinical management. Using functional genomic approaches, we previously characterized HGBCL and NOS, that demonstrate gene expression profiling (GEP), and genetic signatures similar to BL. Herein, we characterize distinct HGBCL, NOS, cohort (n = 55) in adults (n = 45) and in children (n = 10), and compared the GEP, genomic DNA copy number (CN), and mutational spectrum with de novo DLBCL (n = 85) and BL (n = 52). This subgroup, representing ~60% of HGBCL, NOS, lack gene‐expression signature of BL and double hit/dark zone lymphoma, but express DLBCL like signatures and are characterized by either GCB‐ or ABC‐like mRNA signatures and exhibit higher genomic complexity, similar to de novo DLBCL, and show alteration in genes regulating B‐cell activation (CD79B, MYD88, PRDM1, TBLIXR1, CARD11), epigenome (KMT2D, TET2) and cell cycle transition (TP53, ASPM). However, recurrent mutations in genes often mutated in BL (DDX3X, GNA13, CCND3), but rare in DLBCL, are also present in HGBCL‐NOS, highlighting genetic heterogeneity. Consistent with mutation spectrum, frequent genomic CN alterations in genes regulating B‐cell activation (del‐PRDM1, gain‐BCL6, ‐REL, ‐STAT3) and cell cycle regulators (del‐TP53, del‐CDKN2A, del‐RB1, gain‐CCND3) were observed. Pediatric cases showed GCB‐DLBCL‐like mRNA signatures, but also featured hallmark mutations of pediatric BL. Frequent oncogenic PIM1 mutations were present in adult HGBCL, NOS. In vitro analyses with pharmacologic or genetic inhibition of PIM1 expression triggered B‐cell activation and NF‐κB‐induced apoptosis, suggesting that PIM1 is a rational therapeutic target.

01 Jan 2025·Physiological Genomics

Comparison of long- and short-rest periods during high-intensity interval exercise on transcriptomic responses in equine skeletal muscle

Article

Author: Takahashi, Kenya ; Takahashi, Yuji ; Ebisuda, Yusaku ; Mukai, Kazutaka ; Kitaoka, Yu ; Hatta, Hideo

This is the first study to address the comparison of transcriptional responses to high-intensity interval exercise with two different rest periods in skeletal muscle. The expression of genes related to metabolic adaptations altered in both conditions, while genes associated with immune and cytokine responses and protein folding and temperature response were varied with the length of the rest period. These results provide evidence for rest duration-specific transcriptional response to high-intensity interval training.

01 Dec 2024·Journal of Biological Chemistry

Receptor-independent regulation of Gα13 by alpha-1-antitrypsin C-terminal peptides

Article

Author: Toyoshima, Fumiko ; Isaka, Yuta ; Liang, Xiaowen ; Kozasa, Tohru ; Ma, Biao ; Maki, Ritsuko ; Okuno, Yasushi ; Kanada, Ryo ; Ishihama, Yasushi ; Matsumoto, Shigeyuki ; Ogata, Kosuke ; Park, Yonghak ; Ohno, Hiroaki ; Arichi, Norihito

Alpha-1-antitrypsin (AAT), a circulating serine protease inhibitor, is an acute inflammatory response protein with anti-inflammatory functions. The C-terminal peptides of AAT are found in various tissues and have been proposed as putative bioactive peptides with multiple functions, but its mechanism of action remains unclear. We previously reported that a mouse AAT C-terminal peptide of 35 amino acids (mAAT-C_1-35) penetrates plasma membrane and associates guanine nucleotide-binding protein subunit alpha 13 (Gα13). Here, we show that mAAT-C_1-35 binds directly to the guanosine diphosphate (GDP)-bound form of Gα13 through the N-terminal region (mAAT-C_1-17), thereby facilitating the interaction of Gα13・GDP with its effector proteins. The minimal sequence (mAAT-C_3-16) and essential amino acid residue (Phe11) of mAAT-C_1-17 were identified as being necessary for this effect. A molecular dynamics simulation for the Gα13・GDP-mAAT-C_1-17 complex model showed that binding of mAAT-C_1-17 to the region surrounded by switch regions of Gα13 stabilizes the flexible switch II and III regions, thereby maintaining their active conformation. In addition, mAAT-C_1-35 activates the Gα13 signalling pathway in cells where Phe11 is required. Our study reveals the structure-based mechanism of action of AAT-C peptides in the regulation of Gα13, and demonstrates that AAT-C peptides represent a biological peptide capable of activating G protein signals in a manner that is independent of G-protein-coupled receptors.

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GNA13

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