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1

Guenal, I., Y. Risler, and B. Mignotte. "Down-regulation of actin genes precedes microfilament network disruption and actin cleavage during p53-mediated apoptosis." Journal of Cell Science 110, no. 4 (1997): 489–95. http://dx.doi.org/10.1242/jcs.110.4.489.

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Inactivation of Simian Virus 40 large T antigen, in cells immortalized with conditional mutants, leads to activation of p53 and apoptosis. We used the mRNA differential display method to identify genes differentially expressed during this process. We found that steady-state levels of mRNA for cytoplasmic actins decreased early during apoptosis. We also showed that, although the steady-state level of the corresponding proteins is not profoundly affected, they are substrates for an interleukin 1-beta converting enzyme (ICE)-like protease activated during the process. However, only a very small f
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2

Jahn, L., J. Sadoshima, A. Greene, C. Parker, K. G. Morgan, and S. Izumo. "Conditional differentiation of heart- and smooth muscle-derived cells transformed by a temperature-sensitive mutant of SV40 T antigen." Journal of Cell Science 109, no. 2 (1996): 397–407. http://dx.doi.org/10.1242/jcs.109.2.397.

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To create muscle cell lines that conditionally differentiate in vitro we introduced a temperature-sensitive SV40 T antigen by retroviral infection into rat aortic smooth muscle cells (SMCs) and neonatal heart-derived cells. After G418 selection cell lines isolated were characterized at permissive (33 degrees C) and non-permissive (39 degrees C) temperatures. [3H]Thymidine uptake showed tht progression through the cell cycle is greatly reduced at 39 degrees C. Cytoskeletal proteins, such as actins and vimentin did not change significantly after temperature shift, while the number of desmin-posi
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3

Lührmann, Anja, Jürgen Thölke, Ingrid Behn, Jens Schumann, Gisa Tiegs, and Sunna Hauschildt. "Immunomodulating Properties of the Antibiotic Novobiocin in Human Monocytes." Antimicrobial Agents and Chemotherapy 42, no. 8 (1998): 1911–16. http://dx.doi.org/10.1128/aac.42.8.1911.

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ABSTRACT We show that the coumeromycin antibiotic novobiocin, a potent inhibitor of ADP ribosylation, prevents lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1), IL-6, and IL-10 secretion in human peripheral blood mononuclear cells. It shares these cytokine-suppressing properties with other inhibitors of ADP ribosylation. We found that novobiocin prevents TNF-α production by inhibiting translation of the TNF-α mRNA. Elevated TNF-α levels in mice treated withd-galactosamine (GalN)-LPS or GalN-TNF were not reduced by novobiocin; however, the drug exhibite
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Tatic, Vujadin, Vladimir Kanjuh, Sasa Rafajlovski, Kristina Kostic, and Dusan Suscevic. "Importance of inflammation in arteriosclerotic plaque destabilization and rupture." Vojnosanitetski pregled 62, no. 9 (2005): 649–53. http://dx.doi.org/10.2298/vsp0509649t.

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Introduction. Although Rudolf Virchow considered arteriosclerosis an inflammatory disease in his book Cellular Pathology published in 1858, the opinion that it was a degenerative arterial disease as a civilization disease prevailed. Nowadays, a great attention has been paid to the inflammatory process in the pathogenesis of arteriosclerosis and particularly in the destabilization and rupture of plaque. Aim. To find out whether T and B lymphocytes, lipid macrophages, vascular smooth muscle and mast cells as well as plaque destabilization and rupture are present in ruptured arteriosclerotic plaq
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5

Fogg, Christiana N. "T cells need nuclear F-actin." Science 363, no. 6423 (2019): 137.22–139. http://dx.doi.org/10.1126/science.363.6423.137-v.

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6

Corre, Isabelle, Manuel Gomez, Susina Vielkind, and Doreen A. Cantrell. "Analysis of Thymocyte Development Reveals That the Gtpase Rhoa Is a Positive Regulator of T Cell Receptor Responses in Vivo." Journal of Experimental Medicine 194, no. 7 (2001): 903–14. http://dx.doi.org/10.1084/jem.194.7.903.

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Loss of function of the guanine nucleotide binding protein RhoA blocks pre-T cell differentiation and survival indicating that this GTPase is a critical signaling molecule during early thymocyte development. Previous work has shown that the Rho family GTPase Rac-1 can initiate changes in actin dynamics necessary and sufficient for pre-T cell development. The present data now show that Rac-1 actions in pre-T cells require Rho function but that RhoA cannot substitute for Rac-1 and induce the actin cytoskeletal changes necessary for pre-T cell development. Activation of Rho is thus not sufficient
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7

Pacifici, Roberto. "T Cells Involvement in PTH Anabolic Actions." Bone 46 (March 2010): S12. http://dx.doi.org/10.1016/j.bone.2010.01.014.

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8

Liu, Y., N. V. Belkina, and S. Shaw. "HIV Infection of T Cells: Actin-in and Actin-out." Science Signaling 2, no. 66 (2009): pe23. http://dx.doi.org/10.1126/scisignal.266pe23.

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9

Chow, K. L., and R. J. Schwartz. "A combination of closely associated positive and negative cis-acting promoter elements regulates transcription of the skeletal alpha-actin gene." Molecular and Cellular Biology 10, no. 2 (1990): 528–38. http://dx.doi.org/10.1128/mcb.10.2.528.

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The chicken skeletal alpha-actin gene promoter region provides at least a 75-fold-greater transcriptional activity in muscle cells than in fibroblasts. The cis-acting sequences required for cell type-restricted expression within this 200-base-pair (bp) region were elucidated by chloramphenicol acetyltransferase assays of site-directed Bg/II linker-scanning mutations transiently transfected into primary cultures. Four positive cis-acting elements were identified and are required for efficient transcriptional activity in myogenic cells. These elements, conserved across vertebrate evolution, incl
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10

Chow, K. L., and R. J. Schwartz. "A combination of closely associated positive and negative cis-acting promoter elements regulates transcription of the skeletal alpha-actin gene." Molecular and Cellular Biology 10, no. 2 (1990): 528–38. http://dx.doi.org/10.1128/mcb.10.2.528-538.1990.

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The chicken skeletal alpha-actin gene promoter region provides at least a 75-fold-greater transcriptional activity in muscle cells than in fibroblasts. The cis-acting sequences required for cell type-restricted expression within this 200-base-pair (bp) region were elucidated by chloramphenicol acetyltransferase assays of site-directed Bg/II linker-scanning mutations transiently transfected into primary cultures. Four positive cis-acting elements were identified and are required for efficient transcriptional activity in myogenic cells. These elements, conserved across vertebrate evolution, incl
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11

Rivera, Jonathan P., and Jose M. Carnate. "Sinonasal Tract Meningioma." Philippine Journal of Otolaryngology-Head and Neck Surgery 32, no. 2 (2018): 60–61. http://dx.doi.org/10.32412/pjohns.v32i2.89.

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A 63-year old Filipino female presented with epistaxis of undisclosed duration. Examination showed a vascular, pulsating, rubbery intranasal mass involving both nasal cavities. The clinical impression was that of a nasal hemangioma. She underwent excision of the tumor and the specimen was sent for histopathologic evaluation.
 
 The specimen consisted of several tan-brown irregular tissue fragments with an aggregate diameter of 2 cm. Microscopic examination showed a cellular spindle cell tumor underneath the respiratory mucosa. (Figure 1) The tumor cells formed a syncytial pattern arr
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12

Muscat, G. E., T. A. Gustafson, and L. Kedes. "A common factor regulates skeletal and cardiac alpha-actin gene transcription in muscle." Molecular and Cellular Biology 8, no. 10 (1988): 4120–33. http://dx.doi.org/10.1128/mcb.8.10.4120.

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The skeletal and cardiac alpha-actin genes are coexpressed in muscle development but exhibit distinctive tissue-specific patterns of expression. We used an in vivo competition assay and an in vitro electrophoretic mobility shift assay to demonstrate that both genes interact with a common trans-acting factor(s). However, there was at least one gene-specific cis-acting sequence in the skeletal alpha-actin gene that interacted with a trans-acting factor which was not rate limiting in the expression of the cardiac alpha-actin gene. The common factor(s) interacted with several cis-acting regions th
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13

Muscat, G. E., T. A. Gustafson, and L. Kedes. "A common factor regulates skeletal and cardiac alpha-actin gene transcription in muscle." Molecular and Cellular Biology 8, no. 10 (1988): 4120–33. http://dx.doi.org/10.1128/mcb.8.10.4120-4133.1988.

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The skeletal and cardiac alpha-actin genes are coexpressed in muscle development but exhibit distinctive tissue-specific patterns of expression. We used an in vivo competition assay and an in vitro electrophoretic mobility shift assay to demonstrate that both genes interact with a common trans-acting factor(s). However, there was at least one gene-specific cis-acting sequence in the skeletal alpha-actin gene that interacted with a trans-acting factor which was not rate limiting in the expression of the cardiac alpha-actin gene. The common factor(s) interacted with several cis-acting regions th
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14

Arce-Sillas, Asiel, Diana Denisse Álvarez-Luquín, Beatriz Tamaya-Domínguez, et al. "Regulatory T Cells: Molecular Actions on Effector Cells in Immune Regulation." Journal of Immunology Research 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/1720827.

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T regulatory cells play a key role in the control of the immune response, both in health and during illness. While the mechanisms through which T regulatory cells exert their function have been extensively described, their molecular effects on effector cells have received little attention. Thus, this revision is aimed at summarizing our current knowledge on those regulation mechanisms on the target cells from a molecular perspective.
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15

Yu, Hong, Dave Leitenberg, Baiyong Li, and Richard A. Flavell. "Deficiency of Small Gtpase Rac2 Affects T Cell Activation." Journal of Experimental Medicine 194, no. 7 (2001): 915–26. http://dx.doi.org/10.1084/jem.194.7.915.

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Rac2 is a hematopoietic-specific GTPase acting as a molecular switch to mediate both transcriptional activation and cell morphological changes. We have examined the effect of Rac2 deficiency during T cell activation. In Rac2−/− T cells, proliferation was reduced upon stimulation with either plate-bound anti-CD3 or T cell receptor–specific antigen. This defect is accompanied with decreased activation of mitogen activated protein kinase extracellular signal–regulated kinase (ERK)1/2 and p38, and reduced Ca2+ mobilization. TCR stimulation–induced actin polymerization is also reduced. In addition,
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16

Kayama, Hisako, and Kiyoshi Takeda. "Polysaccharide A of Bacteroides fragilis: Actions on Dendritic Cells and T Cells." Molecular Cell 54, no. 2 (2014): 206–7. http://dx.doi.org/10.1016/j.molcel.2014.04.002.

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17

Short, Ben. "Actin works both sides of the immunological synapse." Journal of Cell Biology 208, no. 4 (2015): 383. http://dx.doi.org/10.1083/jcb.2084if.

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18

Karlik, C. C., D. L. Saville, and E. A. Fyrberg. "Two missense alleles of the Drosophila melanogaster act88F actin gene are strongly antimorphic but only weakly induce synthesis of heat shock proteins." Molecular and Cellular Biology 7, no. 9 (1987): 3084–91. http://dx.doi.org/10.1128/mcb.7.9.3084-3091.1987.

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We have characterized two extant mutations of the flight muscle-specific act88F actin gene of Drosophila melanogaster. Both defective alleles were recovered from flightless mutants isolated previously (K. Mogami and Y. Hotta, Mol. Gen. Genet. 183:409-417, 1981). By directly sequencing the mutant alleles, we demonstrated that in act88FIfm(3)2 a single G-C to A-T transition converted arginine-28 to cysteine and that in act88FIfm(3)4 a single A-T to T-A transversion changed isoleucine-76 to phenylalanine. We showed that the actins encoded by either allele were strongly antimorphic. Mutant alleles
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19

Wang, Weifeng, Jia Guo, Dongyang Yu, Paul J. Vorster, WanJun Chen, and Yuntao Wu. "A Dichotomy in Cortical Actin and Chemotactic Actin Activity between Human Memory and Naive T Cells Contributes to Their Differential Susceptibility to HIV-1 Infection." Journal of Biological Chemistry 287, no. 42 (2012): 35455–69. http://dx.doi.org/10.1074/jbc.m112.362400.

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Human memory and naive CD4 T cells can mainly be identified by the reciprocal expression of the CD45RO or CD45RA isoforms. In HIV-1 infection, blood CD45RO memory CD4 T cells are preferentially infected and serve as a major viral reservoir. The molecular mechanism dictating this differential susceptibility to HIV-1 remains largely obscure. Here, we report that the different susceptibility of memory and naive T cells to HIV is not determined by restriction factors such as Apobec3G or BST2. However, we observed a phenotypic distinction between human CD45RO and CD45RA resting CD4 T cells in their
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20

Ramsay, Alan G., Dong-Xia Xing, William K. Decker, et al. "Compared to Adult Peripheral Blood T Cells, Cord Blood T Cells Show Enhanced Immunological Recognition of Chronic Lymphocytic Leukemia Tumor Cells." Blood 112, no. 11 (2008): 2333. http://dx.doi.org/10.1182/blood.v112.11.2333.2333.

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Abstract Following allogeneic stem cell transplantation (SCT) and donor lymphocyte infusion (DLI) from adult peripheral blood (APB), chronic lymphocytic leukemia (CLL) cells are good targets of a graft-versus-leukemia effect. However, some patients eligible for this treatment do not have a suitable allogeneic donor and CLL B cells have been shown to be dysfunctional antigen-presenting cells (APCs) for allogeneic APB T cells. As a result, allogeneic APB T cells show suppressed immunological synapse formation with CLL cells. Umbilical cord blood (CB) is a promising source of hematopoietic cells
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21

AHMED, J. S., P. WIEGERS, H. RITZ, H. HARTWIG, E. SCHEIN, and L. SCHNITTGER. "Generation of Cytotoxic T Lymphocytes and Cytostatic Acting Cells in T. annulata-Immune Cattle." Annals of the New York Academy of Sciences 916, no. 1 (2006): 595–99. http://dx.doi.org/10.1111/j.1749-6632.2000.tb05342.x.

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22

Tamzalit, Fella, Mitchell S. Wang, Weiyang Jin, et al. "Interfacial actin protrusions mechanically enhance killing by cytotoxic T cells." Science Immunology 4, no. 33 (2019): eaav5445. http://dx.doi.org/10.1126/sciimmunol.aav5445.

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Cytotoxic T lymphocytes (CTLs) kill by forming immunological synapses with target cells and secreting toxic proteases and the pore-forming protein perforin into the intercellular space. Immunological synapses are highly dynamic structures that boost perforin activity by applying mechanical force against the target cell. Here, we used high-resolution imaging and microfabrication to investigate how CTLs exert synaptic forces and coordinate their mechanical output with perforin secretion. Using micropatterned stimulatory substrates that enable synapse growth in three dimensions, we found that per
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23

Colin-York, Huw, Sudha Kumari, Liliana Barbieri, Lena Cords, and Marco Fritzsche. "Distinct actin cytoskeleton behaviour in primary and immortalised T-cells." Journal of Cell Science 133, no. 5 (2019): jcs232322. http://dx.doi.org/10.1242/jcs.232322.

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24

Lam Hui, King, Sae In Kwak, and Arpita Upadhyaya. "Adhesion-dependent modulation of actin dynamics in Jurkat T cells." Cytoskeleton 71, no. 2 (2013): 119–35. http://dx.doi.org/10.1002/cm.21156.

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25

IM, Young-jin, Yun-kyung LEE, Hae-young CHUNG, and Dong-soon IM. "Multiple actions of lysophosphatidylcholine in human Jurkat T cells1." Acta Pharmacologica Sinica 27, no. 6 (2006): 700–707. http://dx.doi.org/10.1111/j.1745-7254.2006.00339.x.

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26

Rudd, Brian D. "Neonatal T Cells: A Reinterpretation." Annual Review of Immunology 38, no. 1 (2020): 229–47. http://dx.doi.org/10.1146/annurev-immunol-091319-083608.

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Neonatal CD4+ and CD8+ T cells have historically been characterized as immature or defective. However, recent studies prompt a reinterpretation of the functions of neonatal T cells. Rather than a population of cells always falling short of expectations set by their adult counterparts, neonatal T cells are gaining recognition as a distinct population of lymphocytes well suited for the rapidly changing environment in early life. In this review, I will highlight new evidence indicating that neonatal T cells are not inert or less potent versions of adult T cells but instead are a broadly reactive
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27

Smoligovets, A. A., A. W. Smith, H. J. Wu, R. S. Petit, and J. T. Groves. "Characterization of dynamic actin associations with T-cell receptor microclusters in primary T cells." Journal of Cell Science 125, no. 3 (2012): 735–42. http://dx.doi.org/10.1242/jcs.092825.

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28

Gough, Nancy R. "New connections: T cell actin dynamics." Science Signaling 9, no. 424 (2016): ec95-ec95. http://dx.doi.org/10.1126/scisignal.aaf8940.

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29

Levine, L. "Actions of vanadate of arachidonic acid metabolism by cells in culture." Prostaglandins 41, no. 1 (1991): 7–19. http://dx.doi.org/10.1016/0090-6980(91)90100-t.

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30

Tanaka, Hiromitsu, Naoko Iguchi, Carlos Egydio de Carvalho, Yuko Tadokoro, Kentaro Yomogida, and Yoshitake Nishimune. "Novel Actin-Like Proteins T-ACTIN 1 and T-ACTIN 2 Are Differentially Expressed in the Cytoplasm and Nucleus of Mouse Haploid Germ Cells." Biology of Reproduction 69, no. 2 (2003): 475–82. http://dx.doi.org/10.1095/biolreprod.103.015867.

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31

Arpin, M., E. Friederich, M. Algrain, F. Vernel, and D. Louvard. "Functional differences between L- and T-plastin isoforms." Journal of Cell Biology 127, no. 6 (1994): 1995–2008. http://dx.doi.org/10.1083/jcb.127.6.1995.

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Fimbrins/plastins are a family of highly conserved actin-bundling proteins. They are present in all eukaryotic cells including yeast, but each isoform displays a remarkable tissue specificity. T-plastin is normally found in epithelial and mesenchymal cells while L-plastin is present in hematopoietic cells. However, L-plastin has been also found in tumor cells of non-hematopoietic origin (Lin, C.-S., R. H. Aebersold, S. B. Kent, M. Varma, and J. Leavitt. 1988. Mol. Cell. Biol. 8:4659-4668; Lin, C.-S., R. H. Aebersold, and J. Leavitt. 1990. Mol. Cell. Biol. 10: 1818-1821). To learn more about th
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32

Hu, Kenneth H., and Manish J. Butte. "T cell activation requires force generation." Journal of Cell Biology 213, no. 5 (2016): 535–42. http://dx.doi.org/10.1083/jcb.201511053.

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Triggering of the T cell receptor (TCR) integrates both binding kinetics and mechanical forces. To understand the contribution of the T cell cytoskeleton to these forces, we triggered T cells using a novel application of atomic force microscopy (AFM). We presented antigenic stimulation using the AFM cantilever while simultaneously imaging with optical microscopy and measuring forces on the cantilever. T cells respond forcefully to antigen after calcium flux. All forces and calcium responses were abrogated upon treatment with an F-actin inhibitor. When we emulated the forces of the T cell using
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33

Ramsay, Alan G., Andrew J. Clear, Alexander Davenport, Rewas Fatah, and John G. Gribben. "Chronic Lymphocytic Leukemia Cells Co-Opt CD200, CD270, CD274 and CD276 to Induce Impaired Actin Polarization At the T Cell Immune Synapse." Blood 118, no. 21 (2011): 802. http://dx.doi.org/10.1182/blood.v118.21.802.802.

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Abstract Abstract 802 We have previously demonstrated that impaired formation of the T cell immunological synapse in response to autologous (auto) antigen-presenting cells (APCs) is a global immunosuppressive mechanism in chronic lymphocytic leukemia (CLL) (J Clin Invest. 2008;118(7):2427-2437). Polymerization of F-actin beneath the area of the T cell:APC contact site generates a structural support for signaling molecules to assemble and regulate appropriate CD4+ T cell activation and cytolytic CD8+ T cell (CTL) effector function. Importantly, direct contact interaction with tumor cells was sh
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34

Orlowski, J., and A. F. Clark. "Androgen metabolism and actions in rat ventral prostate epithelial and stromal cell cultures." Biochemistry and Cell Biology 64, no. 6 (1986): 583–93. http://dx.doi.org/10.1139/o86-081.

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The rat ventral prostate requires androgens for normal development, growth, and function. To investigate the relationship between androgen metabolism and its effects in the prostate and to examine differences between the epithelial and stromal cells, we have established a system of primary cell cultures of immature rat ventral prostate cells. Cultures of both cell types after reaching confluency (6–7 days) actively metabolized 3H-labelled testosterone (T), 5α-dihydrotestosterone (5α-DHT), 5α-androstane-3α,17β-diol, and 5α-androstane-3β,17β-diol. The epithelial cells actively reduced T to 5α-DH
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35

Ramsay, Alan G., Abigail M. Lee, and John G. Gribben. "Impaired Actin Polymerization Results in Defective Immunological Synapse Formation in T Cells in Chronic Lymphocytic Leukemia." Blood 110, no. 11 (2007): 338. http://dx.doi.org/10.1182/blood.v110.11.338.338.

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Abstract Cancer is associated with immune deficiency, but the molecular basis for this is poorly defined. We have previously demonstrated that multiple gene expression abnormalities are induced in patients with chronic lymphocytic leukemia (CLL) including defects within the actin cytoskeleton formation pathways. Based on this data, we hypothesized that failure of actin polymerization would result in defects in the formation of the immunological synapse (IS) which is critical for T cell activation and effector function. To assess this, actin polymerization at the IS in T cells in response to su
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36

Lafuente, Esther M., Mathew Salanga, Yoshiko Iwamoto, Lequn Li, and Vassiliki A. Boussiotis. "RIAM Regulates Actin Reorganization at the Immunological Synapse and Calcium Mobilization during T Cell Activation." Blood 108, no. 11 (2006): 1722. http://dx.doi.org/10.1182/blood.v108.11.1722.1722.

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Abstract Engagement of immune recognition subunits on lymphocytes results in cytoskeletal reorganization, polarization of polymerized actin, conjugate formation between T cells and APC, stabilization of the immunological synapse (IS), and initiation of signaling cascades leading to T cell activation. Actin remodeling is essential for these events and is mandatory for T cell activation. We have identified RIAM, a novel adaptor molecule that interacts specifically with active GTP-bound Rap1 and with regulators of the actin cytoskeleton Evl, VASP and Profilin. Profilin associates with G-actin and
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37

Kelleher, J. F., S. J. Atkinson, and T. D. Pollard. "Sequences, structural models, and cellular localization of the actin-related proteins Arp2 and Arp3 from Acanthamoeba." Journal of Cell Biology 131, no. 2 (1995): 385–97. http://dx.doi.org/10.1083/jcb.131.2.385.

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We cloned and sequenced the two actin-related proteins (Arps) present in the profilin-binding complex of Acanthamoeba (Machesky, L. M., S. J. Atkinson, C. Ampe, J. Vandekerckhove, and T. D. Pollard. 1994, J. Cell Biol. 127:107-115). The sequence of Arp2 is more similar to other Arp2s than to actin, while the sequence of Arp3 is more similar to other Arp3s than to actin. Phylogenetic analysis of all known Arps demonstrates that most group into three major families, which are likely to be shared across all eukaryotic phyla. Together with conventional actins, the Arps form a larger family distinc
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38

Ishii, N., N. Moriguchi, and H. Nakajima. "Requirement for early-acting, antigen-specific initiating cells in DNFB contact sensitivity." Journal of Dermatological Science 4, no. 2 (1992): 118. http://dx.doi.org/10.1016/0923-1811(92)90124-t.

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39

Finkelstein, Lisa D., and Pamela L. Schwartzberg. "Tec kinases: shaping T-cell activation through actin." Trends in Cell Biology 14, no. 8 (2004): 443–51. http://dx.doi.org/10.1016/j.tcb.2003.07.001.

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40

Villalba, Martin, Kun Bi, Fernando Rodriguez, Yoshihiko Tanaka, Stephen Schoenberger, and Amnon Altman. "Vav1/Rac-dependent actin cytoskeleton reorganization is required for lipid raft clustering in T cells." Journal of Cell Biology 155, no. 3 (2001): 331–38. http://dx.doi.org/10.1083/jcb.200107080.

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Formation of the immunological synapse (IS) in T cells involves large scale molecular movements that are mediated, at least in part, by reorganization of the actin cytoskeleton. Various signaling proteins accumulate at the IS and are localized in specialized membrane microdomains, known as lipid rafts. We have shown previously that lipid rafts cluster and localize at the IS in antigen-stimulated T cells. Here, we provide evidence that lipid raft polarization to the IS depends on an intracellular pathway that involves Vav1, Rac, and actin cytoskeleton reorganization. Thus, lipid rafts did not t
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41

Ramsay, Alan G., Andrew J. Clear, Rewas Fatah, and John G. Gribben. "Multiple inhibitory ligands induce impaired T-cell immunologic synapse function in chronic lymphocytic leukemia that can be blocked with lenalidomide: establishing a reversible immune evasion mechanism in human cancer." Blood 120, no. 7 (2012): 1412–21. http://dx.doi.org/10.1182/blood-2012-02-411678.

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Abstract Cancer immune evasion is an emerging hallmark of disease progression. We have demonstrated previously that impaired actin polymerization at the T-cell immunologic synapse is a global immune dysfunction in chronic lymphocytic leukemia (CLL). Direct contact with tumor cells induces defective actin polarization at the synapse in previously healthy T cells, but the molecules mediating this dysfunction were not known. In the present study, we show via functional screening assays that CD200, CD270, CD274, and CD276 are coopted by CLL cells to induce impaired actin synapse formation in both
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42

Suzuki, Jun-ichiro, Sho Yamasaki, Jennifer Wu, Gary A. Koretzky, and Takashi Saito. "The actin cloud induced by LFA-1–mediated outside-in signals lowers the threshold for T-cell activation." Blood 109, no. 1 (2006): 168–75. http://dx.doi.org/10.1182/blood-2005-12-020164.

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Abstract The dynamic rearrangement of the actin cytoskeleton plays critical roles in T-cell receptor (TCR) signaling and immunological synapse (IS) formation in T cells. Following actin rearrangement in T cells upon TCR stimulation, we found a unique ring-shaped reorganization of actin called the “actin cloud,” which was specifically induced by outside-in signals through lymphocyte function–associated antigen-1 (LFA-1) engagement. In T-cell–antigen-presenting cell (APC) interactions, the actin cloud is generated in the absence of antigen and localized at the center of the T-cell–APC interface,
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43

Cassimeris, L., D. Safer, V. T. Nachmias, and S. H. Zigmond. "Thymosin beta 4 sequesters the majority of G-actin in resting human polymorphonuclear leukocytes." Journal of Cell Biology 119, no. 5 (1992): 1261–70. http://dx.doi.org/10.1083/jcb.119.5.1261.

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Thymosin beta 4 (T beta 4), a 5-kD peptide which binds G-actin and inhibits its polymerization (Safer, D., M. Elzinga, and V. T. Nachmias. 1991. J. Biol. Chem. 266:4029-4032), appears to be the major G-actin sequestering protein in human PMNs. In support of a previous study by Hannappel, E., and M. Van Kampen (1987. J. Chromatography. 397:279-285), we find that T beta 4 is an abundant peptide in these cells. By reverse phase HPLC of perchloric acid supernatants, human PMNs contain approximately 169 fg/cell +/- 90 fg/cell (SD), corresponding to a cytoplasmic concentration of approximately 149 +
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Na, Bo-Ra, Hye-Ran Kim, Indre Piragyte, et al. "TAGLN2 regulates T cell activation by stabilizing the actin cytoskeleton at the immunological synapse." Journal of Cell Biology 209, no. 1 (2015): 143–62. http://dx.doi.org/10.1083/jcb.201407130.

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The formation of an immunological synapse (IS) requires tight regulation of actin dynamics by many actin polymerizing/depolymerizing proteins. However, the significance of actin stabilization at the IS remains largely unknown. In this paper, we identify a novel function of TAGLN2—an actin-binding protein predominantly expressed in T cells—in stabilizing cortical F-actin, thereby maintaining F-actin contents at the IS and acquiring LFA-1 (leukocyte function-associated antigen-1) activation after T cell receptor stimulation. TAGLN2 blocks actin depolymerization and competes with cofilin both in
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Apollonio, Benedetta, Mariam Fanous, Mohamed-Reda Benmebarek, et al. "CC-122 Repairs T Cell Activation in Chronic Lymphocytic Leukemia That Results in a Concomitant Increase in PD-1:PD-L1 and CTLA-4 Immune Checkpoint Expression at the Immunological Synapse." Blood 126, no. 23 (2015): 1738. http://dx.doi.org/10.1182/blood.v126.23.1738.1738.

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Abstract Immunomodulatory drugs (IMiDs®) such as lenalidomide and immune checkpoint blockade (ICB) antibodies can enhance autologous anti-tumor T cell immunity and have the potential to elicit durable control of disease in B cell malignancies. These immunotherapies are likely to be most effective when employed in treatment combinations. Thus, the goal of pre-clinical research should be to reveal mechanisms of action (MOA) in the tumor microenvironment (TME) and identify biomarkers to guide development of combination therapy for patients. CC-122 is a novel first-in-class pleiotropic pathway mod
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Hou, Tim Y., Jennifer M. Monk, Yang-Yi Fan, et al. "n−3 polyunsaturated fatty acids suppress phosphatidylinositol 4,5-bisphosphate-dependent actin remodelling during CD4+ T-cell activation." Biochemical Journal 443, no. 1 (2012): 27–37. http://dx.doi.org/10.1042/bj20111589.

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n−3 PUFA (polyunsaturated fatty acids), i.e. DHA (docosahexaenoic acid), found in fish oil, exhibit anti-inflammatory properties; however, the molecular mechanisms remain unclear. Since PtdIns(4,5)P2 resides in raft domains and DHA can alter the size of rafts, we hypothesized that PtdIns(4,5)P2 and downstream actin remodelling are perturbed by the incorporation of n−3 PUFA into membranes, resulting in suppressed T-cell activation. CD4+ T-cells isolated from Fat-1 transgenic mice (membranes enriched in n−3 PUFA) exhibited a 50% decrease in PtdIns(4,5)P2. Upon activation by plate-bound anti-CD3/
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Giganti, A. "Actin-filament cross-linking protein T-plastin increases Arp2/3-mediated actin-based movement." Journal of Cell Science 118, no. 6 (2005): 1255–65. http://dx.doi.org/10.1242/jcs.01698.

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Haneda, Masakazu, Ryuichi Kikkawa, Masaki Togawa, Daisuke Koya, Nobuyuki Kajiwara, and Yukio Shigeta. "Metabolic actions of insulin-like growth factor I in cultured glomerular mesangial cells." Metabolism 40, no. 12 (1991): 1311–16. http://dx.doi.org/10.1016/0026-0495(91)90034-t.

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Rivas, Fabiola V., James P. O'Keefe, Maria-Luisa Alegre, and Thomas F. Gajewski. "Actin Cytoskeleton Regulates Calcium Dynamics and NFAT Nuclear Duration." Molecular and Cellular Biology 24, no. 4 (2004): 1628–39. http://dx.doi.org/10.1128/mcb.24.4.1628-1639.2004.

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ABSTRACT T-cell activation by antigen-presenting cells is accompanied by actin polymerization, T-cell receptor (TCR) capping, and formation of the immunological synapse. However, whether actin-dependent events are required for T-cell function is poorly understood. Herein, we provide evidence for an unexpected negative regulatory role of the actin cytoskeleton on TCR-induced cytokine production. Disruption of actin polymerization resulted in prolonged intracellular calcium elevation in response to anti-CD3, thapsigargin, or phorbol myristate acetate plus ionomycin, leading to persistent NFAT (n
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D'Elios, Mario Milco, Marisa Benagiano, Chiara Della Bella, and Amedeo Amedei. "T-cell response to bacterial agents." Journal of Infection in Developing Countries 5, no. 09 (2011): 640–45. http://dx.doi.org/10.3855/jidc.2019.

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T-cell responses are crucial for the outcome of any infection. The type of effector T-cell reaction is determined by a complex interaction of antigen-presenting cells with naive T cells and involves genetic and environmental factors, including the type of antigen, cytokines, chemokines, co-stimulatory molecules, and signalling cascades. The decision for the immune response to go in a certain direction is based not on one signal alone, but rather on many different elements acting both synergistically and antagonistically, and through feedback loops leading to activation or inhibition of T cells
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