Relevant bibliographies by topics / Local Lamellipodia

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Local Lamellipodia'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Local Lamellipodia"

1

Helfand, Brian T., Melissa G. Mendez, S. N. Prasanna Murthy, et al. "Vimentin organization modulates the formation of lamellipodia." Molecular Biology of the Cell 22, no. 8 (2011): 1274–89. http://dx.doi.org/10.1091/mbc.e10-08-0699.

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Vimentin intermediate filaments (VIF) extend throughout the rear and perinuclear regions of migrating fibroblasts, but only nonfilamentous vimentin particles are present in lamellipodial regions. In contrast, VIF networks extend to the entire cell periphery in serum-starved or nonmotile fibroblasts. Upon serum addition or activation of Rac1, VIF are rapidly phosphorylated at Ser-38, a p21-activated kinase phosphorylation site. This phosphorylation of vimentin is coincident with VIF disassembly at and retraction from the cell surface where lamellipodia form. Furthermore, local induction of phot
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2

Adderley, Shaquria P., Curtis Lawrence, Eyong Madonia, Joseph O. Olubadewo, and Jerome W. Breslin. "Histamine activates p38 MAP kinase and alters local lamellipodia dynamics, reducing endothelial barrier integrity and eliciting central movement of actin fibers." American Journal of Physiology-Cell Physiology 309, no. 1 (2015): C51—C59. http://dx.doi.org/10.1152/ajpcell.00096.2015.

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The role of the actin cytoskeleton in endothelial barrier function has been debated for nearly four decades. Our previous investigation revealed spontaneous local lamellipodia in confluent endothelial monolayers that appear to increase overlap at intercellular junctions. We tested the hypothesis that the barrier-disrupting agent histamine would reduce local lamellipodia protrusions and investigated the potential involvement of p38 mitogen-activated protein (MAP) kinase activation and actin stress fiber formation. Confluent monolayers of human umbilical vein endothelial cells (HUVEC) expressing
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3

Nagata-Ohashi, Kyoko, Yusaku Ohta, Kazumichi Goto, et al. "A pathway of neuregulin-induced activation of cofilin-phosphatase Slingshot and cofilin in lamellipodia." Journal of Cell Biology 165, no. 4 (2004): 465–71. http://dx.doi.org/10.1083/jcb.200401136.

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Cofilin mediates lamellipodium extension and polarized cell migration by stimulating actin filament dynamics at the leading edge of migrating cells. Cofilin is inactivated by phosphorylation at Ser-3 and reactivated by cofilin-phosphatase Slingshot-1L (SSH1L). Little is known of signaling mechanisms of cofilin activation and how this activation is spatially regulated. Here, we show that cofilin-phosphatase activity of SSH1L increases ∼10-fold by association with actin filaments, which indicates that actin assembly at the leading edge per se triggers local activation of SSH1L and thereby stimul
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4

Breslin, Jerome W., Xun E. Zhang, Rebecca A. Worthylake, and Flavia M. Souza-Smith. "Involvement of Local Lamellipodia in Endothelial Barrier Function." PLOS ONE 10, no. 2 (2015): e0117970. http://dx.doi.org/10.1371/journal.pone.0117970.

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5

Paul, Nikki R., Jennifer L. Allen, Anna Chapman та ін. "α5β1 integrin recycling promotes Arp2/3-independent cancer cell invasion via the formin FHOD3". Journal of Cell Biology 210, № 6 (2015): 1013–31. http://dx.doi.org/10.1083/jcb.201502040.

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Invasive migration in 3D extracellular matrix (ECM) is crucial to cancer metastasis, yet little is known of the molecular mechanisms that drive reorganization of the cytoskeleton as cancer cells disseminate in vivo. 2D Rac-driven lamellipodial migration is well understood, but how these features apply to 3D migration is not clear. We find that lamellipodia-like protrusions and retrograde actin flow are indeed observed in cells moving in 3D ECM. However, Rab-coupling protein (RCP)-driven endocytic recycling of α5β1 integrin enhances invasive migration of cancer cells into fibronectin-rich 3D EC
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6

Leyman, Shirley, Mazen Sidani, Laila Ritsma, et al. "Unbalancing the Phosphatidylinositol-4,5-bisphosphate–Cofilin Interaction Impairs Cell Steering." Molecular Biology of the Cell 20, no. 21 (2009): 4509–23. http://dx.doi.org/10.1091/mbc.e09-02-0121.

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Cofilin is a key player in actin dynamics during cell migration. Its activity is regulated by (de)phosphorylation, pH, and binding to phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2]. Here, we here use a human cofilin-1 (D122K) mutant with increased binding affinity for PI(4,5)P2 and slower release from the plasma membrane to study the role of the PI(4,5)P2–cofilin interaction in migrating cells. In fibroblasts in a background of endogenous cofilin, D122K cofilin expression negatively affects cell turning frequency. In carcinoma cells with down-regulated endogenous cofilin, D122K cofilin neit
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7

Diefenbach, Thomas J., Vaughan M. Latham, Dean Yimlamai, Canwen A. Liu, Ira M. Herman, and Daniel G. Jay. "Myosin 1c and myosin IIB serve opposing roles in lamellipodial dynamics of the neuronal growth cone." Journal of Cell Biology 158, no. 7 (2002): 1207–17. http://dx.doi.org/10.1083/jcb.200202028.

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The myosin family of motor proteins is implicated in mediating actin-based growth cone motility, but the roles of many myosins remain unclear. We previously implicated myosin 1c (M1c; formerly myosin Iβ) in the retention of lamellipodia (Wang et al., 1996). Here we address the role of myosin II (MII) in chick dorsal root ganglion neuronal growth cone motility and the contribution of M1c and MII to retrograde F-actin flow using chromophore-assisted laser inactivation (CALI). CALI of MII reduced neurite outgrowth and growth cone area by 25%, suggesting a role for MII in lamellipodial expansion.
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8

Liu, Yi-Jun, Ting Zhang, Daxiao Cheng, et al. "Late endosomes promote microglia migration via cytosolic translocation of immature protease cathD." Science Advances 6, no. 50 (2020): eaba5783. http://dx.doi.org/10.1126/sciadv.aba5783.

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Organelle transport requires dynamic cytoskeleton remodeling, but whether cytoskeletal dynamics are, in turn, regulated by organelles remains elusive. Here, we demonstrate that late endosomes, a type of prelysosomal organelles, facilitate actin-cytoskeleton remodeling via cytosolic translocation of immature protease cathepsin D (cathD) during microglia migration. After cytosolic translocation, late endosome–derived cathD juxtaposes actin filaments at the leading edge of lamellipodia. Suppressing cathD expression or blocking its cytosolic translocation impairs the maintenance but not the initia
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9

Taha, Abdallah Abu, Muna Taha, Jochen Seebach, and Hans-J. Schnittler. "ARP2/3-mediated junction-associated lamellipodia control VE-cadherin–based cell junction dynamics and maintain monolayer integrity." Molecular Biology of the Cell 25, no. 2 (2014): 245–56. http://dx.doi.org/10.1091/mbc.e13-07-0404.

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Maintenance and remodeling of endothelial cell junctions critically depend on the VE-cadherin/catenin complex and its interaction with the actin filament cytoskeleton. Here we demonstrate that local lack of vascular endothelial (VE)-cadherin at established cell junctions causes actin-driven and actin-related protein 2/3 complex (ARP2/3)–controlled lamellipodia to appear intermittently at those sites. Lamellipodia overlap the VE-cadherin–free adjacent plasma membranes and facilitate formation of new VE-cadherin adhesion sites, which quickly move into the junctions, driving VE-cadherin dynamics
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10

Martinelli, Roberta, Masataka Kamei, Peter T. Sage, et al. "Release of cellular tension signals self-restorative ventral lamellipodia to heal barrier micro-wounds." Journal of Cell Biology 201, no. 3 (2013): 449–65. http://dx.doi.org/10.1083/jcb.201209077.

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Basic mechanisms by which cellular barriers sense and respond to integrity disruptions remain poorly understood. Despite its tenuous structure and constitutive exposure to disruptive strains, the vascular endothelium exhibits robust barrier function. We show that in response to micrometer-scale disruptions induced by transmigrating leukocytes, endothelial cells generate unique ventral lamellipodia that propagate via integrins toward and across these “micro-wounds” to close them. This novel actin remodeling activity progressively healed multiple micro-wounds in succession and changed direction
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Dissertations / Theses on the topic "Local Lamellipodia"

1

Zhang, Xun E. "S1P-Mediated Endothelial Barrier Enhancement: Role of Rho Family GTPases and Local Lamellipodia." Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/6987.

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The endothelial cells lining the inner surface of the tissue capillaries and post-capillary venules form a semi-permeable barrier between the blood circulation and interstitial compartments. The semi-permeable barrier in these vessels is the major site of blood-tissue exchange. A compromised endothelial barrier contributes to the pathological process such as edema, acute respiratory distress syndrome (ARDS) and tumor metastasis. Sphingosine-1-phosphate (S1P), an endogenous, bioactive lipid present in all cells, is a potential therapeutic agent that can restore compromised endothelial barrier f
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