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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
The hyaluronan receptor RHAMM regulates extracellular-regulated kinase
No full textThis article is hosted on a website external to the CBCRA Open Access Archive. Selecting “View/Open” below will launch the full-text article in another browser window.We have identified two RHAMM (receptor for hyaluronan-mediated motility) isoforms that encode an alternatively spliced exon 4 (Hall, C. L., Yang, B., Yang, X., Zhang, S., Turley, M., Samuel, S., Lange, L. A., Wang, C., Curpen, G. D., Savani, R. C., Greenberg, A. H., and Turley, E. A. (1995) Cell 82, 19-26 and Wang, C., Entwistle, J., Hou, G., Li, Q., and Turley, E. A. (1996) Gene 174, 299-306). One of these, RHAMM variant 4 (RHAMMv4), is transforming when overexpressed and regulates Ras signaling (Hall et al.). Here we note using flow cytometry and confocal analysis that RHAMM isoforms encoding exon 4 occur both on the cell surface and in the cytoplasm. Epitope-tagging experiments indicate that RHAMMv4 occurs only in the cytoplasm. Several observations suggest that both cell surface RHAMM isoforms and RHAMMv4 are involved in regulating extracellular-regulated kinase (ERK) activity. Affinity-purified anti-RHAMM exon 4 antibodies block the ability of platelet-derived growth factor to activate ERK, and these reagents modify the protein tyrosine phosphorylation profile of proteins resulting from treatment with platelet-derived growth factor. A dominant negative form of RHAMMv4 inhibits mutant active Ras activation of ERK and coimmunoprecipitates with both mitogen-activated protein kinase kinase and ERK, suggesting that the intracellular RHAMMv4 acts downstream of Ras, possibly at the level of mitogen-activated protein kinase kinase-ERK interactions. Consistent with this, overexpression of RHAMMv4 constitutively activates ERK. These results identify a novel mechanism for the regulation of the Ras-ERK signaling pathway and suggest that RHAMM plays multiple roles in this regulation
The hyaluronan receptor RHAMM regulates extracellular-regulated kinase
No full textThis article is hosted on a website external to the CBCRA Open Access Archive. Selecting “View/Open” below will launch the full-text article in another browser window.We have identified two RHAMM (receptor for hyaluronan-mediated motility) isoforms that encode an alternatively spliced exon 4 (Hall, C. L., Yang, B., Yang, X., Zhang, S., Turley, M., Samuel, S., Lange, L. A., Wang, C., Curpen, G. D., Savani, R. C., Greenberg, A. H., and Turley, E. A. (1995) Cell 82, 19-26 and Wang, C., Entwistle, J., Hou, G., Li, Q., and Turley, E. A. (1996) Gene 174, 299-306). One of these, RHAMM variant 4 (RHAMMv4), is transforming when overexpressed and regulates Ras signaling (Hall et al.). Here we note using flow cytometry and confocal analysis that RHAMM isoforms encoding exon 4 occur both on the cell surface and in the cytoplasm. Epitope-tagging experiments indicate that RHAMMv4 occurs only in the cytoplasm. Several observations suggest that both cell surface RHAMM isoforms and RHAMMv4 are involved in regulating extracellular-regulated kinase (ERK) activity. Affinity-purified anti-RHAMM exon 4 antibodies block the ability of platelet-derived growth factor to activate ERK, and these reagents modify the protein tyrosine phosphorylation profile of proteins resulting from treatment with platelet-derived growth factor. A dominant negative form of RHAMMv4 inhibits mutant active Ras activation of ERK and coimmunoprecipitates with both mitogen-activated protein kinase kinase and ERK, suggesting that the intracellular RHAMMv4 acts downstream of Ras, possibly at the level of mitogen-activated protein kinase kinase-ERK interactions. Consistent with this, overexpression of RHAMMv4 constitutively activates ERK. These results identify a novel mechanism for the regulation of the Ras-ERK signaling pathway and suggest that RHAMM plays multiple roles in this regulation
Differential Acquisition of m-Sequences using Recursive Soft Sequential Estimation
No full textIn this contribution a novel sequential estimation method is proposed for the acquisition of -sequences. This sequential estimation method exploits the principle of iterative soft-in-soft-out (SISO) decoding for enhancing the acquisition performance, and that of differential pre-processing for the sake of achieving an enhanced acquisition performance, when communicating over various communication environments. Hence the advocated acquisition arrangement is referred to as the Differential Recursive Soft Sequential Estimation (DRSSE) acquisition scheme. The DRSSE acquisition scheme exhibits a low complexity, which is similar to that of an -sequence generator, while achieving an acquisition time that is linearly dependent on the number of stages in the -sequence generator. A low acquisition time is achieved with the advent of the property that the proposed DRSSE scheme is capable of determining the real-time reliabilities associated with the decision concerning a set of, say , consecutive chips. This set of consecutive chips constitutes the sufficient initial condition for enabling the local -sequence generator to produce a synchronized local despreading -sequence replica. Owing to these attractive characteristics, the DRSSE acquisition scheme constitutes a promising initial synchronization scheme for acquisition of long -sequences, when communicating over various propagation environments
∑_(l+m=k,l,m≥0) ((α+l-1)¦l) ((β+m-1)¦m)=((α+β+k-1)¦k) and its application to negative binomial distribution
No full textWe prove here the following equation: ∑_(l+m=k,l,m≥0) ((α+l-1)¦l) ((β+m-1)¦m)=((α+β+k-1)¦k) and give its application to prove the reproductive property of the negative binomial distribution.
These finite sum equation involving binomial coefficients and proof of the reproductive property are not known as far as the author knows.論文(Article)departmental bulletin pape
De Maiestate / Praeside M. Jacobo Thomasio, Moralis Philosoph. P. P., publice disputabit Johannes Dunte, R. L. Author & Respon: ad diem 9. Septembr. H L. Q. C.
No full textDE MAIESTATE / PRAESIDE M. JACOBO THOMASIO, MORALIS PHILOSOPH. P. P., PUBLICE DISPUTABIT JOHANNES DUNTE, R. L. AUTHOR & RESPON: AD DIEM 9. SEPTEMBR. H L. Q. C.
De Maiestate / Praeside M. Jacobo Thomasio, Moralis Philosoph. P. P., publice disputabit Johannes Dunte, R. L. Author & Respon: ad diem 9. Septembr. H L. Q. C. (1)
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Erratum to: Effect of moderate red wine intake on cardiac prognosis after recent acute myocardial infarction of subjects with Type 2 diabetes mellitus (Diabetic Medicine, (2006), 23, 9, (974-981), 10.1111/j.1464-5491.2006.01886.x)
No full textIn an article by Marfella et al, the author name C. Saron is incorrect and should be listed as C. Sardu. Therefore the correct author list is: R. Marfella, F. Cacciapuoti, M. Siniscalchi, F. C. Sasso, F. Marchese, F. Cinone, E. Musacchio, M. A. Marfella, L. Ruggiero, G. Chiorazzo, D. Liberti, G. Chiorazzo, G. F. Nicoletti, C. Sardu, F. D'Andrea, C. Ammendola, M. Verza and L. Coppola.In an article by Marfella et al, the author name C. Saron is incorrect and should be listed as C. Sardu. Therefore the correct author list is: R. Marfella, F. Cacciapuoti, M. Siniscalchi, F. C. Sasso, F. Marchese, F. Cinone, E. Musacchio, M. A. Marfella, L. Ruggiero, G. Chiorazzo, D. Liberti, G. Chiorazzo, G. F. Nicoletti, C. Sardu, F. D'Andrea, C. Ammendola, M. Verza and L. Coppola
Doing it differently: Engaging interview participants with imaginative variation
No full textImaginative variation was identified by Husserl (1936/1970) as a phenomenological technique for the purpose of elucidating the manner in which phenomena appear to consciousness. Briefly, by engaging in the phenomenological reduction and using imaginative variation, phenomenologists are able to describe the experience of consciousness, having stepped outside of the natural attitude through the epochē. Imaginative variation is a stage aimed at explicating the structures of experience, and is best described as a mental experiment. Features of the experience are imaginatively altered in order to view the phenomenon under investigation from varying perspectives. Husserl argued that this process will reveal the essences of an experience, as only those aspects that are invariant to the experience of the phenomenon will not be able to change through the variation.
Often in qualitative research interviews, participants struggle to articulate or verbalise their experiences. The purpose of this article is to detail a radical and novel way of using imaginative variation with interview participants, by asking the participants to engage with imaginative variation, in order to produce a rich and insightful experiential account of a phenomenon. We will discuss how the first author successfully used imaginative variation in this way in her study of the erotic experience of bondage, discipline, dominance & submission, and sadism & masochism (BDSM), before considering the usefulness of this technique when applied to areas of study beyond sexuality
Informetrics on M. N. Srinivas
No full textM. N. Srinivas, the well known sociologist is widely recognised as architect of modern Indian sociology and social anthropology. His publications have been analysed by year, domain, authorship pattern, channels of communication used. Keywords, etc. The results indicate that the papers published by him are of a nature that qualify him to be a 'role model' for the younger generations to emulate.
By the end of 1995, Srinivas had to his credit 144 papers which, included 33 broad papers in sociology and anthropology; 18 papers in social change; 28 papers in village studies; 12 papers on religion; 17 papers on caste and 36 papers of general popular interest. The periods 1958-61 and 1974-77, when Srinivas was 38-41 and 58-61 years old. were his most productive periods with highest publication activity
The stability of IQ in people with low intellectual ability: an analysis of the literature
No full textA meta-analysis of the stability of low IQ (IQ 80) was performed on IQ tests that have been
commonly used—tests that were derived by D. Wechsler (1949, 1955, 1974, 1981, 1991, 1997)
and those based on the Binet scales (L. M. Terman, 1960; L. M. Terman & Merrill, 1972). Weighted-
mean stability coefficients of .77 and .78 were found for Verbal IQ (V IQ) and Performance IQ
(P IQ) on the Wechsler tests and .82 for Full-Scale IQ (FS IQ) on both Wechsler and Binet tests,
for a mean test–retest interval of 2.8 years. Although the majority of FS IQs changed by less than
6 points, 14% changed by 10 points or more. The author suggests that the results of IQ assessment
should be treated with more caution than previously thought
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