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Articular Cartilage Development
Published in Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi, Articular Cartilage, 2017
Kyriacos A. Athanasiou, Eric M. Darling, Grayson D. DuRaine, Jerry C. Hu, A. Hari Reddi
Rho family small GTPases are activated by switching from an inactive GDP-bound molecule to an active GTP-bound form. Switching to the active form is controlled by guanine nucleotide exchange factors (GEFs), while switching to the inactive form is regulated by GTPase activating proteins (GAPs). GEFs and GAPs are under the control of a multitude of cell surface receptors, including integrins, serine/threonine and tyrosine kinase receptors, and GPCRs. They link extracellular matrix signaling to changes in the cytoskeleton and cell shape.
Introduction to Cell Biology
Published in Anthony R. Mundy, John M. Fitzpatrick, David E. Neal, Nicholas J. R. George, The Scientific Basis of Urology, 2010
Once detached from its neighbors, a cell migrates by the formation of transient sites of interaction with the extracellular matrix, called focal adhesions. The focal adhesion complex comprises a multitude of different proteins such as Fak, Src, and paxillin, and acts to bridge extracellular matrix–bound integrins to the actin cytoskeleton. Focal adhesions are linked to stress fibers composed of actin and myosin, which in turn provide the mechanical contractility to promote cell migration. The coordinated activity of proteins of the Rho family of GTPases act at the leading edge of the migrating cell to reorganize actin filaments, generating protrusive finger-like (filopodia) and sheet-like (lamellipodia) structures, while also stimulating contraction at the rear of the cell by regulating the assembly of acto-myosin filaments. In this manner, the signals generated at focal adhesions promote the directional migration of the cell. Migrating cells can also secrete proteases such as matrix metalloproteases (MMPs) to degrade the local matrix and provide space into which the cell can move.
Genetics of NF1 and NF2
Published in J. K. Cowell, Molecular Genetics of Cancer, 2003
Margaret R. Wallace, Mia MacCollin
On the basis of sequence similarity, the NF2 protein product was determined to be a member of the protein 4.1 family of cytoskeleton associated proteins (Figure 5). This was an unexpected finding, since no other family members are associated with tumor formation and only one, protein 4.1 itself, is associated with human genetic disease (hereditary elliptocytosis). The ERM proteins (ezrin, moesin, radixin), to which the NF2 protein is most closely related, share 70 to 75% amino acid identity and a common structure. These proteins localize to motile regions of the cell, including microvilli, cellular protrusions and leading and ruffling edges. ERM proteins interact with the Rho family of GTPases in a signaling cascade which controls the organization of the spectrin-actin cytoskeleton and cell adhesion. Although less is currently known about NF2 protein physiology and function than about other ERM family members, similar interactions with the cytoskeleton are beginning to be identified.
Clinical significance of serum CDC42 in the prediction of uremic vascular calcification incidence and progression
Published in Libyan Journal of Medicine, 2023
Mingzhi Xu, Mingjiao Pan, Na An, Ruman Chen, Yafei Bai, Jiqing He, Chunli Wang, Yonghui Qi
The Rho family of GTPases emerges as vital molecules that tune-fine the structures and functions of kidney cell types, thus affecting kidney physiology and diseases [8]. Cell division cycle 42 (CDC42), one of the best characterized members of the Rho family of GTPases, plays a role in the regulation of various cell functions, such as cytoskeletal architecture, polarity, cytokinesis, proliferation, and migration [9–12]. Depletion of CDC42 triggers injury of vascular endothelial cells and inhibits vascular endothelial growth factor A-mediated vascular sprouting from aortic rings, contributing to the defect in vasculature formation of various organs [13]. Meanwhile, CDC42 modulates epithelial cell polarity and the actin cytoskeleton to participate in kidney epithelial tubulogenesis [14]. The deficiency of CDC42 results in a disruption of renal ciliogenesis and a polycystic kidney disease phenotype in zebrafish and mice [15]. The role of CDC42 in cartilage development and calcified tissue formation has also been reported [16]. Most importantly, the recruitment of CDC42 promotes VC in the context of CKD by upregulating the expression of bone-related factors [17]. However, the role and expression patterns of CDC42 in uremia have not been discussed before.
Evaluation of myopia-associated genes in a Han Chinese population with high myopia
Published in Ophthalmic Genetics, 2023
Zhenzhen Liu, Guangqi An, Yadan Huo, Youmei Xu, Pengyi Zhou, Kunpeng Xie, Haiyan Zhu, Bo Jin, Liping Du, Xuemin Jin
Among the other newly identified genes, AKAP13 on 15q25.3 encodes a member of the A-kinase anchoring protein family, functions as adaptor proteins to regulate Rho signaling, and is a guanine nucleotide exchange factor for RhoA-GTPases (17). The Rho family of GTPases plays a vital role in the nervous system (18). FRMD4B on 3p14.1 encodes a protein that interacts with cytohesin-3 and functions as a scaffolding protein (2). A recent study suggested the role of the FRMD4B-ecytohesin-3 complex as a key player in influencing cell junction dynamics in the retina and contributing to the regulation of the growth and development of photoreceptor cells (19). It is the first report in a Chinese population to identify an association between rs72748160 and rs74633073 with high myopia and obtain a negative result.
Down regulation of DNA topoisomerase IIβ exerts neurodegeneration like effect through Rho GTPases in cellular model of Parkinson’s disease by Down regulating tyrosine hydroxylase
Published in Neurological Research, 2021
Kiyak Bercem Yeman, Sevim Isik
Rho family of GTPases are known to regulate the actin cytoskeleton, transcriptional activation, membrane trafficking, and microtubule dynamics [13]. These proteins can therefore regulate the morphology of neurites and growth cones during neural development. The best-characterized members of this family are RhoA, Rac1, and Cdc42 [9,13]. Rac1/Cdc42 and RhoA typically show an antagonistic association with neuronal morphology. While Rac1 and Cdc42 enhance growth cone development and neurite outgrowth, RhoA regulates neurite outgrowth negatively inducing growth cone collapse and neurite retraction during neural development [14]. Therefore, Rho GTPases have been proposed to be involved in PD [15–17]. It is believed that these proteins can be used to reverse the long-standing damage of the nigrostriatal degeneration and can potentially be modulated in PD therapy [12].