STI1 antagonizes cytoskeleton collapse mediated by small GTPase Rnd1 and regulates neurite growth

Souza, Luiz Eduardo Rizzo de; Costa, Michele D.M.; Bilek, Evandro Santos; Lopes, Marilene H.; Martins, Vilma R.; Püschel, Andreas W.; Mercadante, Adriana F.; Nakao, Lia S.; Zanata, Sı́lvio M.

doi:10.1016/j.yexcr.2014.03.017

Cited by 17 publications

(13 citation statements)

References 50 publications

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“…Hop is also required for neurosphere self-renewal and differentiation in neuronal cells which is linked to neuronal development and conceptual processes such as memory (Coitinho et al 2007). These findings are consistent with recent evidence that Hop interacts with Rnd1 GTPase to enhance neurite outgrowth in neuronal cell lines, leading to the proposal that Hop may be involved in neuronal development (de Souza et al 2014).…”

Section: Developmental and Protein Folding Disorderssupporting

confidence: 92%

Hsp70/Hsp90 Organising Protein (Hop): Beyond Interactions with Chaperones and Prion Proteins

Baindur-Hudson

Edkins

Blatch

2014

Subcellular Biochemistry

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The Hsp70/Hsp90 organising protein (Hop), also known as stress-inducible protein 1 (STI1), has received considerable attention for diverse cellular functions in both healthy and diseased states. There is extensive evidence that intracellular Hop is a co-chaperone of the major chaperones Hsp70 and Hsp90, playing an important role in the productive folding of Hsp90 client proteins. Consequently, Hop is implicated in a number of key signalling pathways, including aberrant pathways leading to cancer. However, Hop is also secreted and it is now well established that Hop also serves as a receptor for the prion protein, PrP(C). The intracellular and extracellular forms of Hop most likely represent two different isoforms, although the molecular determinants of these divergent functions are yet to be identified. There is also a growing body of research that reports the involvement of Hop in cellular activities that appear independent of either chaperones or PrP(C). While Hop has been shown to have various cellular functions, its biological function remains elusive. However, recent knockout studies in mammals suggest that Hop has an important role in embryonic development. This review provides a critical overview of the latest molecular, cellular and biological research on Hop, critically evaluating its function in healthy systems and how this function is adapted in diseases states.

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Section: Developmental and Protein Folding Disorderssupporting

confidence: 92%

Hsp70/Hsp90 Organising Protein (Hop): Beyond Interactions with Chaperones and Prion Proteins

Baindur-Hudson

Edkins

Blatch

2014

Subcellular Biochemistry

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“…We found that ZIKV induced Rnd1 and ARHGAP26Rho in infected hBMECs, which direct brain capillary permeability (56, 57). These findings suggested potential mechanisms for ZIKV to permeabilize and spread across the BBB.…”

Section: Discussionmentioning

confidence: 88%

“…ZIKV also induced apoptosis-inhibitory and -regulating factors IAP2 and XAF1 (55) 5- to 201-fold (1 to 9 dpi) (Table 1). Two genes associated with cell permeability, Rnd1, a constitutively activated Rho GTPase (56), and ARHGAP26, a Rho-activating factor (57), were also induced in ZIKV-infected hBMECs. Chemokine CCL5/RANTES was highly induced (40- to 2,327-fold) 1 to 9 dpi, along with a subset of moderately induced CXCL10/11 and CCL20 chemokines (Table 1) (GEO GSE98889).…”

Section: Resultsmentioning

confidence: 99%

Zika Virus Persistently Infects and Is Basolaterally Released from Primary Human Brain Microvascular Endothelial Cells

Mladinich

Schwedes

Mackow

2017

mBio

103

139

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Zika virus (ZIKV) is a mosquito-borne Flavivirus that has emerged as the cause of encephalitis and fetal microencephaly in the Americas. ZIKV uniquely persists in human bodily fluids for up to 6 months, is sexually transmitted, and traverses the placenta and the blood-brain barrier (BBB) to damage neurons. Cells that support persistent ZIKV replication and mechanisms by which ZIKV establishes persistence remain enigmatic but central to ZIKV entry into protected neuronal compartments. The endothelial cell (EC) lining of capillaries normally constrains transplacental transmission and forms the BBB, which selectively restricts access of blood constituents to neurons. We found that ZIKV (strain PRVABC59) persistently infects and continuously replicates in primary human brain microvascular ECs (hBMECs), without cytopathology, for >9 days and following hBMEC passage. ZIKV did not permeabilize hBMECs but was released basolaterally from polarized hBMECs, suggesting a direct mechanism for ZIKV to cross the BBB. ZIKV-infected hBMECs were rapidly resistant to alpha interferon (IFN-α) and transiently induced, but failed to secrete, IFN-β and IFN-λ. Global transcriptome analysis determined that ZIKV constitutively induced IFN regulatory factor 7 (IRF7), IRF9, and IFN-stimulated genes (ISGs) 1 to 9 days postinfection, despite persistently replicating in hBMECs. ZIKV constitutively induced ISG15, HERC5, and USP18, which are linked to hepatitis C virus (HCV) persistence and IFN regulation, chemokine CCL5, which is associated with immunopathogenesis, as well as cell survival factors. Our results reveal that hBMECs act as a reservoir of persistent ZIKV replication, suggest routes for ZIKV to cross hBMECs into neuronal compartments, and define novel mechanisms of ZIKV persistence that can be targeted to restrict ZIKV spread.

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“… 1 (Foster et al, 1996 ), 2 (Wennerberg et al, 2003 ), 3 (Pacary et al, 2011 ), 4 (Azzarelli et al, 2014 ) 5 (Riento et al, 2003 ), 6 (Riento et al, 2005 ), 7 (Goh and Manser, 2010 ), 8 (Naud et al, 2003 ), 9 (Miller and Bement, 2009 ), 10 (Oinuma et al, 2003 ), 11 (Oinuma et al, 2004 ), 12 (Uesugi et al, 2009 ), 13 (Rohm et al, 2000 ), 14 (Toyofuku et al, 2005 ), 15 (Zanata et al, 2002 ), 16 (Fujita et al, 2002 ), 17 (Wakita et al, 2011 ), 18 (Tanaka et al, 2002 ), 19 (Karaulanov et al, 2009 ), 20 (Ogata et al, 2007 ), 21(Tanaka et al, 2006 ), 22 (Li et al, 2009 ), 23 (Katoh et al, 2002 ), 24 (Harada et al, 2005 ), 25 (Vayssiere et al, 2000 ), 26 (De Souza et al, 2014 ) . …”

Section: Molecular Mechanisms Mediating Rnd Activity In Migrating Neumentioning

confidence: 99%

Function and regulation of Rnd proteins in cortical projection neuron migration

Azzarelli

Guillemot²,

Pacary

2015

Front. Neurosci.

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The mammalian cerebral cortex contains a high variety of neuronal subtypes that acquire precise spatial locations and form long or short-range connections to establish functional neuronal circuits. During embryonic development, cortical projection neurons are generated in the areas lining the lateral ventricles and they subsequently undergo radial migration to reach the position of their final maturation within the cortical plate. The control of the neuroblast migratory behavior and the coordination of the migration process with other neurogenic events such as cell cycle exit, differentiation and final maturation are crucial to normal brain development. Among the key regulators of cortical neuron migration, the small GTP binding proteins of the Rho family and the atypical Rnd members play important roles in integrating intracellular signaling pathways into changes in cytoskeletal dynamics and motility behavior. Here we review the role of Rnd proteins during cortical neuronal migration and we discuss both the upstream mechanisms that regulate Rnd protein activity and the downstream molecular pathways that mediate Rnd effects on cell cytoskeleton.

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STI1 antagonizes cytoskeleton collapse mediated by small GTPase Rnd1 and regulates neurite growth

Cited by 17 publications

References 50 publications

Hsp70/Hsp90 Organising Protein (Hop): Beyond Interactions with Chaperones and Prion Proteins

Hsp70/Hsp90 Organising Protein (Hop): Beyond Interactions with Chaperones and Prion Proteins

Zika Virus Persistently Infects and Is Basolaterally Released from Primary Human Brain Microvascular Endothelial Cells

Function and regulation of Rnd proteins in cortical projection neuron migration

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