Cytohesin-2/ARNO, through Its Interaction with Focal Adhesion Adaptor Protein Paxillin, Regulates Preadipocyte Migration via the Downstream Activation of Arf6

Torii, Tomohiro; Miyamoto, Yuki; Sanbe, Atsushi; Nishimura, Kohji; Yamauchi, Junji; Tanoue, Akito

doi:10.1074/jbc.m110.125658

Cited by 56 publications

(49 citation statements)

References 56 publications

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“…ARNO) to the plasma membrane, 41 and cytohesin-2, in turn, interacts with the focal contact protein paxillin. 42 We, therefore, argue that, in the absence of Lmx1b, podocytes contain a stiffer actin cytoskeleton, which may make the podocytes more vulnerable. A similar scenario has been proposed for the mechanism underlying hereditary forms of FSGS caused by mutations in ACTN4.…”

Section: Discussionmentioning

confidence: 99%

LMX1B is Essential for the Maintenance of Differentiated Podocytes in Adult Kidneys

Burghardt

Kastner

Suleiman

et al. 2013

Journal of the American Society of Nephrology

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Mutations of the LMX1B gene cause nail-patella syndrome, a rare autosomal-dominant disorder affecting the development of the limbs, eyes, brain, and kidneys. The characterization of conventional Lmx1b knockout mice has shown that LMX1B regulates the development of podocyte foot processes and slit diaphragms, but studies using podocyte-specific Lmx1b knockout mice have yielded conflicting results regarding the importance of LMX1B for maintaining podocyte structures. In order to address this question, we generated inducible podocyte-specific Lmx1b knockout mice. One week of Lmx1b inactivation in adult mice resulted in proteinuria with only minimal foot process effacement. Notably, expression levels of slit diaphragm and basement membrane proteins remained stable at this time point, and basement membrane charge properties also did not change, suggesting that alternative mechanisms mediate the development of proteinuria in these mice. Cell biological and biophysical experiments with primary podocytes isolated after 1 week of Lmx1b inactivation indicated dysregulation of actin cytoskeleton organization, and time-resolved DNA microarray analysis identified the genes encoding actin cytoskeleton-associated proteins, including Abra and Arl4c, as putative LMX1B targets. Chromatin immunoprecipitation experiments in conditionally immortalized human podocytes and gel shift assays showed that LMX1B recognizes AT-rich binding sites (FLAT elements) in the promoter regions of ABRA and ARL4C, and knockdown experiments in zebrafish support a model in which LMX1B and ABRA act in a common pathway during pronephros development. Our report establishes the importance of LMX1B in fully differentiated podocytes and argues that LMX1B is essential for the maintenance of an appropriately structured actin cytoskeleton in podocytes.

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Section: Discussionmentioning

confidence: 99%

LMX1B is Essential for the Maintenance of Differentiated Podocytes in Adult Kidneys

Burghardt

Kastner

Suleiman

et al. 2013

Journal of the American Society of Nephrology

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“…Arl4D plays a role in activating cytohesin-2/ARNO and Arf6, thus acting as a novel regulator of actin reorganization (15,19). Interestingly, cytohesin-2/ARNO and Arf6 control the migration of 3T3-L1 preadipocytes (20). During adipogenesis, adipocytes morphologically change from fibroblastic cells to round, lipid-laden cells.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of the small GTPase Arl4D suppresses adipogenesis

Ka²,

Kwon³

et al. 2011

Int J Mol Med

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Abstract. Arl4D is a developmentally-regulated member of the ADP-ribosylation factor/ARF-like protein (ARF/Arl) family of Ras-related GTPases. Although Arl4 protein is reported to be expressed in adipose tissue, the function of Arl4D is unknown. To investigate the potential role of Arl4D in adipogenesis, we examined Arl4D expression during adipocyte differentiation and the effects of Arl4D overexpression on adipogenesis. Arl4D protein increased early in adipogenesis, with the highest expression at 4 h after adipogenesis initiation, followed by a decrease thereafter. Overexpression of Arl4D in 3T3-L1 cells potently inhibited their ability to differentiate and accumulate lipid, and reduced the expression of adipogenic genes. Furthermore, treatment with valproic acid, an Arl4D inducer, suppressed adipogenesis. These results suggest that rapid reduction of Arl4D is required for adipogenesis to proceed.

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“…Accumulating evidences demonstrated that Arf6GEF regulates Arf6 activation and its downstream effectors control activity of various intracellular signal molecules during cell migration ( Figure 1B) (Santy and Casanova 2001, Palacios and D'Souza-Schorey 2003, Torii et al 2010. In particular, it is well known that Arf6GEF cytohesin-1 and cytohesin-2 control cell migration.…”

Section: Switching Arf6 Signal Through Arf6gef and Arf6gap Controls Cmentioning

confidence: 99%

“…For example, cytohesin-associated scaffold protein (CASP)/Cybr/cytohesin-interacting protein (CYTIP) (Mansour et al 2002, Tang et al 2002, Boehm et al 2003, interaction protein for cytohesin exchange factor (IPCEF)/KIAA0403 (Venkateswarlu 2003), RLIP76/RalBP1 (Lee et al 2014), ADP-ribosylation factor-like protein 4D (Arl4D) (Hofmann et al 2007, Li et al 2007), paxillin (Torii et al 2010), actinin-1 and CCDC120 ) are known as cytohesin interacting protein.…”

Section: Cytohesin-2 Binding Proteinsmentioning

confidence: 99%

A new signalsome containing cytohesin-2 and CCDC120 controls neurite outgrowth

Torii

Yamauchi

2015

MRAJ

Self Cite

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Many functions in the nervous system depend on neural morphological changes including the cell polarity and neurite outgrowth and propagation of action potentials through networks of neuron-neuron and neuron-glia. Previous studies demonstrated that these associations are necessary for small GTPases activation in neurons. Especially, it is well known that small GTPases play a key role in neurite outgrowth, which is one of the most important events in neuronal development. Recent studies also have identified and characterized that molecular mechanisms of membrane trafficking and actin cytoskeleton formation/reorganization in migrating cells mediated by ADP-ribosylation factor 6 (Arf6) and its regulator cytohesin-2 are required for cell migration and neurite outgrowth. However, it have not completely established yet whether Arf6 activation is necessary or not in molecular mechanisms of neurite outgrowth. Our recent studies first identified and characterized that the previous unknown functional coiled-coil containing protein 120 (CCDC120) binds to cytohesin-2 and coordinately regulates neurite outgrowth in neuronal cells. This review summarizes the process that has been made in our understanding about the necessity of Arf6 activation in neurite outgrowth and the signaling transduction including cytohesin-2-CCDC120 complex in neuronal cells.

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Cytohesin-2/ARNO, through Its Interaction with Focal Adhesion Adaptor Protein Paxillin, Regulates Preadipocyte Migration via the Downstream Activation of Arf6

Cited by 56 publications

References 56 publications

LMX1B is Essential for the Maintenance of Differentiated Podocytes in Adult Kidneys

LMX1B is Essential for the Maintenance of Differentiated Podocytes in Adult Kidneys

Overexpression of the small GTPase Arl4D suppresses adipogenesis

A new signalsome containing cytohesin-2 and CCDC120 controls neurite outgrowth

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