1,391 research outputs found
TGF-beta 1 stimulation of cell locomotion utilizes the hyaluronan receptor RHAMM and hyaluronan.
No full textTGF-beta is a potent stimulator of motility in a variety of cell types. It has recently been shown that hyaluronan (HA) can directly promote locomotion of cells through interaction with the HA receptor RHAMM. We have investigated the role of RHAMM and HA in TGF-beta-stimulated locomotion and show that TGF-beta triggers the transcription, synthesis and membrane expression of the RHAMM receptor and the secretion of HA coincident with the induction of the locomotory response. This was demonstrated by both incubating cells with exogenous TGF-beta1 and by stimulating the production of bioactive TGF-beta1 in tumor cells transfected with TGF-beta1 under the control of the metallothionein promoter. TGF-beta1-induced locomotion was suppressed by antibodies that prevented HA/RHAMM interaction, using polyclonal antibodies to either RHAMM fusion protein or RHAMM peptides, or mAbs to purified RHAMM. Peptides corresponding to the HA-binding motif of RHAMM also suppressed TGF-beta1-induced increases in motility rate. Spontaneous locomotion of fibrosarcoma cells was blocked by neutralizing secreted TGF-beta with panspecific TGF-beta antibodies and by inhibition of TGF-beta1 secretion with antisense oligonucleotides. Polyclonal anti-RHAMM fusion protein antibodies and peptide from the RHAMM HA-binding motif also suppressed the spontaneous motility rate of fibrosarcoma cells. These data suggest that fibrosarcoma cell locomotion requires TGF-beta, and the pathway by which TGF-beta stimulates locomotion uses the HA receptor RHAMM and HA.PT: J; CR: ALLEN JB, 1990, J EXP MED, V171, P231 ANZANO MA, 1985, MOL CELL BIOL, V5, P242 BARNARD JA, 1990, BIOCHIM BIOPHYS ACTA, V1032, P79 BASSOLS A, 1988, J BIOL CHEM, V263, P3039 BRAY BA, 1991, AM REV RESPIR DIS, V143, P284 CHAN BM, 1992, CELL, V68, P1051 CHEN JK, 1987, P NATL ACAD SCI USA, V84, P5287 CULTY M, 1990, J CELL BIOL 1, V111, P2765 DALAL BI, 1993, AM J PATHOL, V143, P381 DANIELPOUR D, 1989, J CELL PHYSIOL, V138, P79 DELPECH B, 1981, J NEUROCHEM, V36, P855 DERYNCK R, 1987, CANCER RES, V47, P707 DOEGE K, 1987, J BIOL CHEM, V262, P17757 FASSEN AE, 1992, J CELL BIOL, V116, P521 FAVA RA, 1991, J EXP MED, V173, P1121 GOETINCK PF, 1987, J CELL BIOL, V105, P2403 GOUGH NM, 1988, ANAL BIOCHEM, V173, P93 HARDWICK C, 1992, J CELL BIOL, V117, P1343 HEINE UI, 1987, J CELL BIOL, V105, P286 HEINO J, 1989, J BIOL CHEM, V264, P380 HELDIN P, 1989, BIOCHEM J, V258, P919 HOOK M, 1984, ANNU REV BIOCHEM, V53, P847 HURTA RAR, 1991, J BIOL CHEM, V266, P24097 HYNES RO, 1992, CELL, V69, P11 KAHARI VM, 1991, J BIOL CHEM, V266, P10608 KHALIL N, 1989, J EXP MED, V170, P727 KHALIL N, 1991, CIBA F SYMP, V157, P194 KIMATA K, 1983, CANCER RES, V43, P1347 KLEINSOYER C, 1989, ARTERIOSCLEROSIS, V9, P147 KRUSIUS T, 1987, J BIOL CHEM, V262, P13120 LAEMMLI UK, 1970, NATURE, V227, P680 LIOTTA LA, 1988, CANCER SURV, V7, P631 MADRI JA, 1988, J CELL BIOL, V106, P1375 MASSAGUE J, 1990, ANNU REV CELL BIOL, V6, P597 MCCARTHY JB, 1992, IN PRESS CRC CRIT RE MCCLARTY GA, 1987, BIOCHEM BIOPH RES CO, V145, P1276 MOORADIAN DL, 1992, J NATL CANCER I, V84, P523 NEAME PJ, 1986, J BIOL CHEM, V261, P3519 NETTELBLADT O, 1989, AM REV RESPIR DIS, V139, P759 NUGENT MA, 1992, J BIOL CHEM, V267, P21256 PARTIN AW, 1988, CANCER RES, V48, P6050 PARTIN AW, 1989, P NATL ACAD SCI USA, V86, P1254 PERIDES G, 1989, J BIOL CHEM, V264, P5981 PEROTTI D, 1991, CANCER RES, V51, P5491 PIERCE GF, 1989, P NATL ACAD SCI USA, V86, P2229 POSTLETHWAITE AE, 1987, J EXP MED, V165, P251 REIBMAN J, 1991, P NATL ACAD SCI USA, V88, P6805 ROBERTS AB, 1990, HDB EXPT PHARM, V95, P419 SAMUEL SK, 1992, EMBO J, V11, P1599 SATO Y, 1988, J CELL BIOL, V107, P1199 SCHOR SL, 1989, IN VITRO CELL DEV B, V25, P737 SCHWARZ LC, 1990, GROWTH FACTORS, V3, P115 STAMENKOVIC I, 1991, EMBO J, V10, P343 STOKER M, 1991, BIOCHIM BIOPHYS ACTA, V1072, P81 THOMAS L, 1992, J CELL BIOL, V118, P971 TOOLE BP, 1979, P NATL ACAD SCI USA, V76, P6299 TOOLE BP, 1989, CIBA F SYMP, V143, P138 TOOLE BP, 1990, CURR OPIN CELL BIOL, V2, P839 TURLEY EA, 1985, CANCER RES, V45, P5098 TURLEY EA, 1985, EXP CELL RES, V161, P17 TURLEY EA, 1987, BIOCHEMISTRY-US, V26, P2997 TURLEY EA, 1989, EXP CELL RES, V181, P340 TURLEY EA, 1991, ADV DRUG DELIVER REV, V7, P257 TURLEY EA, 1991, J CELL BIOL, V112, P1041 WAHL SM, 1987, P NATL ACAD SCI USA, V84, P5788 WELSH DR, 1991, P NATL ACAD SCI USA, V87, P7678 YAMADA KM, 1990, CANCER RES, V50, P4485 YAMAGUCHI Y, 1990, NATURE, V346, P281 YANG BH, 1993, J BIOL CHEM, V268, P8617; NR: 69; TC: 73; J9: J CELL BIOL; PG: 10; GA: ME817Source type: Electronic(1
Carta informando sobre el estado de las misiones de California, 1776 diciembre 25
No full textCarta informando sobre el estado de las misiones de California, específicamente las Misiones de San Diego, San Juan Capistrano y Santa Clara, y la fuerza militar según noticias que el autor ha recibido de correspondencia anterior. El autor señala la suspensión de la reconstrucción de la Misión de San Diego en ruinas después de la revuelta, recomendando clemencia para los líderes de la rebelión. El autor también solicita el establecimiento de la Misión Santa Clara cerca del Presidio de San Francisco, indicando los suministros necesarios para la fundación. —— Letter informing on the state of the California missions, specifically Missions San Diego, San Juan Capistrano, and Santa Clara, and the military force per news the author has received from prior correspondence. The author notes the suspension of the reconstruction of the ruined Mission of San Diego after the revolt, recommending clemency for the leaders of the rebellion. The author also requests the establishment of Mission Santa Clara near the Presidio of San Francisco, indicating the necessary supplies for the founding. 2 f. (4 p.
Band
No full text[1903] Group Picture. [on back] Back row: Charles Reed; Frederick Ruble; Harlie Innis; H. C. Tilley (leader); Norris Pollard; F. E. Montandon. Center row: C. E. Bolles; Anthony VanHarten; W. C. Turley; F. B. Costello; R. W. Fisher. Front row: J. H. Miller; G. E. Horton; A. K. Carlson
The zoo as ecotourism attraction – visitor reactions, perceptions and management implications: the case of Hamilton Zoo, New Zealand
No full textThis paper reports results from a survey of 359 visitors to Hamilton Zoo, New Zealand. The questionnaire comprised items relating to motives for visiting the zoo, and evaluations of attributes, thereby permitting an importance-evaluation approach. The construction of the questionnaire was prompted by zoo management wishing to learn more about what motivated visits, and whether there were perceived deficiencies in visitors' experiences of the zoo. Like other studies (e.g. Turley, 2001) it was concluded that zoos represent an opportunity for family-based trips. However, while some opportunities exist for learning, on the whole visitors were not generally interested in acquiring detailed information about wildlife. Indeed, more importance was attached to the viewing of animals than to the recognition that possibly animals might require 'private places'. These findings prompt a discussion about the extent to which zoos might be able to replace or supplement trips to natural habitats as a means of viewing animals, and concludes that for this to happen significant changes in zoo layout would be required. Additionally, possible implications for zoo management are discussed
Role of Delta-like 4 in Jagged1-induced tumour angiogenesis and tumour growth
No full textDelta-like 4 (DLL4) and Jagged1 (JAG1) are two key Notch ligands implicated in tumour angiogenesis. They were shown to have opposite effects on mouse retinal and adult regenerative angiogenesis. In tumours, both ligands are upregulated but their relative effects and interactions in tumour biology, particularly in tumour response to therapeutic intervention are unclear. Here we demonstrate that DLL4 and JAG1 displayed equal potency in stimulating Notch target genes in HMEC-1 endothelial cells but had opposing effects on sprouting angiogenesis in vitro. Mouse DLL4 or JAG1 expressed in glioblastoma cells decreased tumour cell proliferation in vitro but promoted tumour growth in vivo. mDLL4-expressing tumours showed fewer but larger vessels whereas mJAG1-tumours produced more vessels. In both tumour types pericyte coverage was decreased but the vessels were more perfused. Both ligands increased tumour resistance towards anti-VEGF therapy but the resistance was higher in mDLL4-tumours versus mJAG1-tumours. However, their sensitivity to the therapy was restored by blocking Notch signalling with dibenzazepine. Importantly, anti- DLL4 antibody blocked the effect of JAG1 on tumour growth and increased vessel branching in vivo. The mechanism behind the differential responsiveness was due to a positive feedback loop for DLL4-Notch signalling, rendering DLL4 more dominant in activating Notch signalling in the tumour microenvironment. We concluded that DLL4 and JAG1 promote tumour growth by modulating tumour angiogenesis via different mechanisms. JAG1 is not antagonistic but utilises DLL4 in tumour angiogenesis. The results suggest that anti-JAG1 therapy should be explored in conjunction with anti- DLL4 treatment in developing anti-Notch therapies in clinics
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Class of 1949 - October
No full textAmpel, D. B. Bell, J. Berland, S. I. Bernsen, S. Coleman, D. H. Farkash, I. Garcia, F. L. Harrison, S. Hirsch, R. K. Knebel, T. L. Lennard, J. H. Livingston, M. R. Maher, F. E. Match, F. Murphy, C. G. Puntervold, S. B. Reiner, J. Rodbell, D. F. Rogal, A. Rush, R. Sacks, H. Schwartz, J. W. Smirlock, I. Smith, A. W. Sosin, J. J. Starkman, M. I. Stone, H. M. Swartz, N. Turley, T. F. Walsh, J. E. Zeldin, S. L. Zucker, J.https://brooklynworks.brooklaw.edu/bls_classphotos/1028/thumbnail.jp
Class of 1949 - October
No full textAmpel, D. B. Bell, J. Berland, S. I. Bernsen, S. Coleman, D. H. Farkash, I. Garcia, F. L. Harrison, S. Hirsch, R. K. Knebel, T. L. Lennard, J. H. Livingston, M. R. Maher, F. E. Match, F. Murphy, C. G. Puntervold, S. B. Reiner, J. Rodbell, D. F. Rogal, A. Rush, R. Sacks, H. Schwartz, J. W. Smirlock, I. Smith, A. W. Sosin, J. J. Starkman, M. I. Stone, H. M. Swartz, N. Turley, T. F. Walsh, J. E. Zeldin, S. L. Zucker, J.https://brooklynworks.brooklaw.edu/bls_classphotos/1028/thumbnail.jp
Class of 1949 - October
No full textAmpel, D. B. Bell, J. Berland, S. I. Bernsen, S. Coleman, D. H. Farkash, I. Garcia, F. L. Harrison, S. Hirsch, R. K. Knebel, T. L. Lennard, J. H. Livingston, M. R. Maher, F. E. Match, F. Murphy, C. G. Puntervold, S. B. Reiner, J. Rodbell, D. F. Rogal, A. Rush, R. Sacks, H. Schwartz, J. W. Smirlock, I. Smith, A. W. Sosin, J. J. Starkman, M. I. Stone, H. M. Swartz, N. Turley, T. F. Walsh, J. E. Zeldin, S. L. Zucker, J.https://brooklynworks.brooklaw.edu/bls_classphotos/1028/thumbnail.jp
Hypoxia regulates FGFR3 expression via HIF-1α and miR-100 and contributes to cell survival in non-muscle invasive bladder cancer
No full textBackground:Non-muscle invasive (NMI) bladder cancer is characterised by increased expression and activating mutations of FGFR3. We have previously investigated the role of microRNAs in bladder cancer and have shown that FGFR3 is a target of miR-100. In this study, we investigated the effects of hypoxia on miR-100 and FGFR3 expression, and the link between miR-100 and FGFR3 in hypoxia.Methods:Bladder cancer cell lines were exposed to normoxic or hypoxic conditions and examined for the expression of FGFR3 by quantitative PCR (qPCR) and western blotting, and miR-100 by qPCR. The effect of FGFR3 and miR-100 on cell viability in two-dimensional (2-D) and three-dimensional (3-D) was examined by transfecting siRNA or mimic-100, respectively.Results:In NMI bladder cancer cell lines, FGFR3 expression was induced by hypoxia in a transcriptional and HIF-1α-dependent manner. Increased FGFR3 was also in part dependent on miR-100 levels, which decreased in hypoxia. Knockdown of FGFR3 led to a decrease in phosphorylation of the downstream kinases mitogen-activated protein kinase (MAPK) and protein kinase B (PKB), which was more pronounced under hypoxic conditions. Furthermore, transfection of mimic-100 also decreased phosphorylation of MAPK and PKB. Finally, knocking down FGFR3 profoundly decreased 2-D and 3-D cell growth, whereas introduction of mimic-100 decreased 3-D growth of cells.Conclusion:Hypoxia, in part via suppression of miR-100, induces FGFR3 expression in bladder cancer, both of which have an important role in maintaining cell viability under conditions of stress. © 2013 Cancer Research UK. All rights reserved
Carta sobre un informe de las misiones de California, 1774 mayo 15
No full textCarta al virrey que acompañaba un informe oficial de fray Francisco Palóu, presidente de las misiones de California. El informe detallaba bautismos, incluidos los de dos jefes indígenas en la misión de San Luis. Verger también proporciona cifras corregidas que muestran 493 bautismos en lugar de los 490 previamente reportados. El informe de Palóu no se incluye con la carta. —— Letter to the viceroy that accompanied an official report from Fray Francisco Palóu, president of the California missions. The report detailed baptisms, including those of two Indigenous chiefs at the Mission of San Luis. Verger also provides corrected figures showing 493 baptisms rather than the previously reported 490. Palóu's report is not with the letter. 1 f. (2 p.
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