Relevant bibliographies by topics / Osteopontiini

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Academic literature on the topic 'Osteopontiini'

Author: Grafiati
Published: 4 June 2021
Last updated: 3 February 2022

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Journal articles on the topic "Osteopontiini"

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Choi, K. W., D. W. Kim, and S. W. Lee. "Purification and Properties of Osteopontin from Bovine Milk." Journal of Animal Science and Technology 45, no. 3 (June 30, 2003): 491–98. http://dx.doi.org/10.5187/jast.2003.45.3.491.

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Chiu, Tai-Jan, Hung-I. Lu, Chang-Han Chen, Wan-Ting Huang, Yu-Ming Wang, Wei-Che Lin, and Shau-Hsuan Li. "Osteopontin Expression Is Associated with the Poor Prognosis in Patients with Locally Advanced Esophageal Squamous Cell Carcinoma Receiving Preoperative Chemoradiotherapy." BioMed Research International 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/9098215.

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Background. The osteopontin has been involved in therapeutic resistance in a variety of cancers. But, the significance of osteopontin expression on the prognosis of patients with locally advanced esophageal squamous cell carcinoma (ESCC) receiving chemoradiotherapy is unclear.Methods.In 80 patients with locally advanced ESCC receiving preoperative chemoradiotherapy between 1999 and 2012, osteopontin expression was evaluated by immunohistochemistry and correlated with treatment outcome. The functional role of osteopontin in ESCC cell lines was determined by osteopontin-mediated siRNA.Results. Osteopontin expression and clinical T4 classification were significantly associated with poor pathological complete response. Univariate analyses demonstrated that osteopontin overexpression and clinical T classification, T4, were significantly associated with worse overall survival and disease-free survival. In multivariate comparison, osteopontin overexpression and clinical T classification, T4, represented the independent adverse prognosticator. In ESCC cell lines, endogenous osteopontin depletion by osteopontin-mediated siRNA increased sensitivity to cisplatin. Osteopontin expression is independently correlated with the response of chemoradiotherapy and prognosis of patients with locally advanced ESCC receiving preoperative chemoradiotherapy.Conclusions. Our results suggest that osteopontin may be a potential therapeutic target for patients with ESCC treated with preoperative chemoradiotherapy.
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Crivello, Joseph F., and E. Delvin. "Isolation and characterization of a cDNA for osteopontin-k: A kidney cell adhesion molecule with high homology to osteopontins." Journal of Bone and Mineral Research 7, no. 6 (December 3, 2009): 693–99. http://dx.doi.org/10.1002/jbmr.5650070614.

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Sodek, J., B. Ganss, and M. D. McKee. "Osteopontin." Critical Reviews in Oral Biology & Medicine 11, no. 3 (July 2000): 279–303. http://dx.doi.org/10.1177/10454411000110030101.

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Osteopontin (OPN) is a highly phosphorylated sialoprotein that is a prominent component of the mineralized extracellular matrices of bones and teeth. OPN is characterized by the presence of a polyaspartic acid sequence and sites of Ser/Thr phosphorylation that mediate hydroxyapatite binding, and a highly conserved RGD motif that mediates cell attachment/signaling. Expression of OPN in a variety of tissues indicates a multiplicity of functions that involve one or more of these conserved motifs. While the lack of a clear phenotype in OPN "knockout" mice has not established a definitive role for OPN in any tissue, recent studies have provided some novel and intriguing insights into the versatility of this enigmatic protein in diverse biological events, including developmental processes, wound healing, immunological responses, tumorigenesis, bone resorption, and calcification. The ability of OPN to stimulate cell activity through multiple receptors linked to several interactive signaling pathways can account for much of the functional diversity. In this review, we discuss the structural features of OPN I hat relate to its function in the formation, remodeling, and maintenance of bones and teeth.
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Scatena, Marta, Lucy Liaw, and Cecilia M. Giachelli. "Osteopontin." Arteriosclerosis, Thrombosis, and Vascular Biology 27, no. 11 (November 2007): 2302–9. http://dx.doi.org/10.1161/atvbaha.107.144824.

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Szalay, Gudrun, Martina Sauter, Michael Haberland, Ulrich Zuegel, Andreas Steinmeyer, Reinhard Kandolf, and Karin Klingel. "Osteopontin." Circulation Research 104, no. 7 (April 10, 2009): 851–59. http://dx.doi.org/10.1161/circresaha.109.193805.

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Shaheen, Mazen, and Neal L. Weintraub. "Osteopontin." Arteriosclerosis, Thrombosis, and Vascular Biology 27, no. 3 (March 2007): 439–41. http://dx.doi.org/10.1161/01.atv.0000258640.30287.7b.

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Demer, Linda L., and Yin Tintut. "Osteopontin." Circulation Research 84, no. 2 (February 5, 1999): 250–52. http://dx.doi.org/10.1161/01.res.84.2.250.

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Chellaiah, M. A., and K. A. Hruska. "Osteopontin." Drug News & Perspectives 11, no. 6 (1998): 350. http://dx.doi.org/10.1358/dnp.1998.11.6.863656.

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Vogt, Mario HJ, Joop ten Kate, Roosmarie JM Drent, Chris H. Polman, and Raymond Hupperts. "Increased osteopontin plasma levels in multiple sclerosis patients correlate with bone-specific markers." Multiple Sclerosis Journal 16, no. 4 (January 19, 2010): 443–49. http://dx.doi.org/10.1177/1352458509359723.

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The pro-inflammatory cytokine osteopontin has been found to be highly expressed in multiple sclerosis lesions and plasma levels are increased during relapses in relapse-onset multiple sclerosis patients. The objective was to determine the relationship between osteopontin plasma and cerebrospinal fluid levels in relation to the immunoglobulin G index. In addition, osteopontin plasma levels were compared with osteopontin mRNA levels in peripheral blood mononuclear cells and bone-specific markers to analyse whether osteopontin may be peripherally produced. Osteopontin and bone-specific markers were determined in paired plasma—cerebrospinal fluid samples and serum samples of relapse-onset multiple sclerosis patients ( n = 36), respectively. Osteopontin mRNA levels were determined by quantitative polymerase chain reaction analysis. Compared to healthy controls ( n = 20), plasma osteopontin levels were significantly increased in relapsing-remitting multiple sclerosis patients and correlated ( r = 0.43, p = 0.013) with the immunoglobulin G index. In contrast, cerebrospinal fluid osteopontin levels correlated neither with plasma osteopontin in paired samples nor with the immunoglobulin G index. Since osteopontin mRNA levels in peripheral blood mononuclear cells of relapsing-remitting multiple sclerosis patients did not correlate with osteopontin plasma levels, peripheral blood mononuclear cells might not be the major source for the increased osteopontin plasma levels. Osteopontin plasma levels correlated ( r = 0.42, p = 0.035) with the bone-specific degradation product C-telopeptide of type-1 collagen. In addition, another immunomodulatory molecule involved in bone metabolism, 25-OH vitamin D, correlated negatively ( r = —0.359, p = 0.048) with the immunoglobulin G index. This study suggests that bone-related molecules like osteopontin and vitamin D with important immunomodulatory functions are related to the immunoglobulin G index in relapsing-remitting multiple sclerosis patients.
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Dissertations / Theses on the topic "Osteopontiini"

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Huusko, T. (Tuija). "Genetic and molecular background of ascending aortic aneurysms." Doctoral thesis, Oulun yliopisto, 2013. http://urn.fi/urn:isbn:9789526201269.

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Abstract Thoracic aortic aneurysms (TAAs) are a significant source of morbidity and mortality. Classical risk factors for TAAs are hypertension, atherosclerosis, male gender, smoking, age, high body mass index, family history and chronic obstructive pulmonary disease. In addition, in certain cases of TAAs, i.e., ascending aortic aneurysms (AscAA), genetic factors are highly prominent. Matrix metalloproteinases are in a major role in the destruction of the aortic wall and the imbalance between matrix metalloproteinases, and their inhibitors are involved in the formation of aneurysms. In addition, osteopontin is a potent regulator of matrix metalloproteinases and it is widely expressed in injured arteries. Recently, telomere shortening has been shown to be involved in the development of abdominal aortic aneurysms (AAA). In this aneurysm type, atherosclerosis has a major role. Since atherosclerosis is frequently absent in the case of TAAs, the length of telomeres was measured in the blood samples of TAA patients. The purpose of this thesis was to study the genetic background of TAAs of the ascending aorta and furthermore, the molecular background of this disease. The first study was done with families with TAAs, and dissections and one chromosomal locus (5q13-14) of the studied seven loci showed a significant genetic linkage for TAAs. Two other studies were done exploiting our TAA case-control material. Study II showed elevated levels of osteopontin, matrix metalloproteinase type 2 and 9 in the plasma and tissue samples of TAA patients compared with controls. In the third study, longer blood leukocyte telomeres were found in the DNA samples of TAA patients compared with controls; furthermore, the elevation of telomere lengthening protein telomerase expression was found in the tissue samples of TAA patients. This thesis presents region 5q13-14 as a potential genetic regulator for TAAs in Finnish families. In addition, elevated levels of osteopontin, matrix metalloproteinase type 2 and 9 can be considered as a plasma biomarker for aneurysmal disease. Furthermore, longer blood leukocytes were found to be a significant risk factor for developing TAAs
Tiivistelmä Rinta-aortan aneurysmat ovat merkittävä sairastumisiin ja kuolemiin johtava tekijä. Perinteisinä riskitekijöinä aneurysmille on pidetty korkeaa verenpainetta, ateroskleroosia, miessukupuolta, tupakointia, ikää, ylipainoa, suvussa esiintyneitä aneurysmatapauksia ja keuhkoahtaumatautia. Näiden lisäksi erityisesti nousevan rinta-aortan alueella esiintyvissä aneurysmissa myös perinnöllisillä tekijöillä on korostunut merkitys. Matriksimetalloproteinaaseilla ja niiden estäjillä on merkittävä rooli, kun aortan seinämää hajotetaan. Tasapainon järkkyminen kyseisten proteiinien keskinäisessä suhteessa voi johtaa aneurysman muodostumiseen. Myös osteopontiinin tiedetään olevan tehokas matriksimetalloproteinaasien säätelijä, ja sitä tuotetaankin yleisesti vahingoittuneessa verisuonessa. Telomeerien lyhentyminen on vastikään yhdistetty vatsa-aortan alueella esiintyviin aneurysmiin, joissa ateroskleroosilla on yleensä merkittävä rooli. Koska ateroskleroosi on vain harvoin nousevan rinta-aortan alueen aneurysmien taustalla, rinta-aortan aneurysmapotilaiden valkosolujen telomeerien suhteelliset pituudet määritettiin. Väitöskirjan ensimmäisessä osatyössä keskityttiin löytämään geneettinen kytkentä rinta-aortan aneurysmien ja jonkin seitsemän tutkitun kromosomialueen välille. Geneettinen kytkentä löydettiin kromosomialueelta 5q13-14. Osatöissä 2 ja 3 hyödynnettiin rinta-aortan aneurysmien potilas- ja verrokkiaineistoja. Osatyö 2 osoitti, että matriksimetalloproteinaasien (2 ja 9) määrät ovat kohonneet rinta-aortan aneurysmapotilaiden näytteissä verrokkeihin verrattuna. Osatyössä 3 telomeerien suhteelliset pituudet veren valkosoluissa olivat pidemmät nousevan rinta-aortan aneurysmapotilaiden näytteissä verrokkihenkilöiden näytteisiin verrattuna. Myös telomeraasin tuotto oli lisääntynyt rinta-aortan aneurysmapotilaiden aorttakudosnäytteissä. Väitöskirjassa esitetään tuloksena kromosomialue 5q13-14 geneettisenä säätelijänä suomalaisissa suvuittain esiintyvissä rinta-aortan aneurysmatapauksissa. Kohonneita matriksimetalloproteinaasien ja osteopontiinin tasoja voidaan lisäksi pitää biomarkkereina rinta-aortan aneurysmien sairastavuudelle. Veren valkosolujen pidemmät telomeerit näyttävät myös olevan yhteydessä rinta-aortan aneurysmien sairastavuuteen
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Luukkonen, J. (Jani). "Osteopontin and osteoclasts in rheumatoid arthritis and osteoarthritis." Doctoral thesis, Oulun yliopisto, 2019. http://urn.fi/urn:isbn:9789526223643.

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Abstract Rheumatoid arthritis and osteoarthritis are two chronic joint diseases, which cause two of the largest socioeconomical burdens among all joint diseases according to the World Health Organization. Both diseases are associated with changes in bone structure and bone cell, especially osteoclast, function. The etiology or pathogenesis of these diseases are not completely understood. Traditionally, osteoarthritis is seen as a disease resulting from mechanical wear of cartilage and bone, and rheumatoid arthritis as an autoinflammatory disease of synovial tissue. However, also in osteoarthritis chronic inflammation is present in synovial tissue, and in rheumatoid arthritis large changes in bone structure are seen. The field of study focusing on this connection between inflammation and bone is called osteoimmunology and it can explain many features of these chronic diseases linking joint health to disturbances in bone homeostasis. Here, the study focused on the function of osteoclasts in normal and pathological environments, and on the factors that have an effect on bone resorption, with a special emphasis on the protein osteopontin. Samples of synovial fluid and serum from rheumatoid arthritis and osteoarthritis patients were analyzed for factors affecting osteoclasts, and in vitro cell cultures of human derived osteoclasts were used to analyze osteoclast function in normal and pathological environment. The phosphorylation of osteopontin was found to be increased in rheumatoid arthritis, along with multiple other inflammatory factors that also affect osteoclasts, such as IL-6, IL-8 and VEGF. Osteoclast cell cultures showed how the use of different patient samples significantly affected osteoclastogenesis, due to so-called inflammatory osteoclastogenesis. Additionally, we show that osteoclasts deposit osteopontin into the resorption lacunae during bone resorption. Based on the results, the inflammatory component present in both osteoarthritis and rheumatoid arthritis significantly affects osteoclast function, and its further study in the future may reveal new therapeutic possibilities. Especially the new discoveries of osteopontin’s role in normal osteoclast function and its changes seen between osteoarthritis and rheumatoid arthritis may prove to have therapeutic potential
Tiivistelmä Nivelreuma ja nivelrikko ovat kroonisia nivelsairauksia, jotka Maailman terveysjärjestön (WHO) mukaan aiheuttavat eniten sosioekonomista haittaa. Molemmissa sairauksissa luiden rakenteessa ja luusolujen, erityisesti osteoklastien, toiminnassa tapahtuu muutoksia. Kummankaan taudin etiologiaa tai patogeneesiä ei täysin tunneta. Perinteisesti ajatellaan, että nivelrikko johtuu rusto- ja luukudoksen mekaanisesta kulumisesta ja nivelreuma nivelkalvon autoinflammatoorisesta tulehduksesta. Kuitenkin nivelrikossa nähdään myös selkeä nivelkalvon krooninen tulehdus ja nivelreumassa suuria luun rakenteen muutoksia. Tutkimusala, joka tutkii tulehduksen ja luun yhteyttä, on nimeltään osteoimmunologia. Tässä väitöskirjassa tutkitaan osteoklastien toimintaa ja niihin vaikuttavia tekijöitä, erityisesti proteiini osteopontiinia, normaalissa ja tautiympäristössä. Analysoin osteoklasteihin vaikuttavia tekijöitä nivelrikko- ja nivelreumapotilaiden näytteistä sekä osteoklastien toimintaa soluviljelmissä. Soluviljelmissä käytettiin nivelreuma- ja nivelrikkopotilaiden näytteitä mahdollisimman totuudenmukaisen ympäristön luomiseksi osteoklasteille. Tutkimuksessa osoitettiin, kuinka osteopontiinin fosforylaatio on lisääntynyt nivelreumapotilaiden nivelnesteessä. Myös useiden muiden osteoklasteihin vaikuttavien tekijöiden, kuten IL-6:n, IL-8:n ja VEGF:n, havaittiin lisääntyneen nivelreumassa. Osteoklastien soluviljelmissä havaittiin selkeät erot siinä, miten eri potilasnäytteet vaikuttavat osteoklasteihin ja erityisesti tulehduksen aiheuttamaan osteoklastien syntyyn. Osoitan myös, miten osteoklastit erittävät osteopontiinia luunhajotuskuoppaan luun hajotuksen aikana. Tutkimustulosten mukaan krooninen tulehdustila nivelrikossa ja nivelreumassa vaikuttaa huomattavasti osteoklastien toimintaan. Uskon, että lisätutkimukset tällä saralla voivat paljastaa uusia hoidollisia mahdollisuuksia. Erityisesti uudet löydökset osteopontiinin roolista osteoklastien toiminnassa sekä muutoksista nivelrikossa ja nivelreumassa vaativat jatkotutkimuksia, jotta proteiinin kliininen merkittävyys saadaan selvitettyä
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Teixeira, Lucas Novaes 1981. "Estudo da expressão de osteopontina em sistemas de coculturas de células osteoblásticas e epiteliais neoplásicas humanas e seus efeitos sobre o fenótipo neoplásico e a ativação osteoclástica." [s.n.], 2015. http://repositorio.unicamp.br/jspui/handle/REPOSIP/288466.

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Orientador: Paulo Tambasco de Oliveira
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba
Made available in DSpace on 2018-08-26T15:44:04Z (GMT). No. of bitstreams: 1 Teixeira_LucasNovaes_D.pdf: 3520593 bytes, checksum: e42a5497740bc09fe80b9a6a035947df (MD5) Previous issue date: 2015
Resumo: O carcinoma espinocelular (CEC) oral representa a neoplasia maligna mais prevalente das estruturas bucais, podendo invadir o tecido ósseo e promover sua reabsorção em até 56% dos casos. A expressão da proteína matricelular osteopontina (OPN) tem sido relacionada a uma maior agressividade de neoplasias malignas, incluindo o CEC oral. No tecido ósseo, a OPN representa a proteína mais abundante da matriz não colágena, concentrada nas interfaces ósseas, i.e. lâminas limitantes, linhas de cimentação e reversas, sendo essencial para adesão e funções de osteoblastos e osteoclastos. Apesar de no microambiente tumoral a OPN estar associada a um fenótipo neoplásico mais agressivo, ainda não está estabelecido o papel da OPN secretada por osteoblastos sobre células neoplásicas derivadas de CEC oral e o impacto sobre osteoclastos. O presente estudo teve como objetivos avaliar a expressão de OPN em sistemas de coculturas de células osteoblásticas e epiteliais neoplásicas malignas humanas e os efeitos da expressão de OPN secretada por osteoblastos sobre o fenótipo neoplásico in vitro. Adicionalmente, avaliou-se o efeito das coculturas sobre a atividade osteoclástica. Células epiteliais neoplásicas malignas derivadas de CEC oral (SCC9) foram plaqueadas sobre membranas de Transwell®, recobertas ou não por uma camada fina e uniforme de Matrigel, e cocultivadas com células osteoblásticas (SAOS-2) durante seu pico de expressão de OPN (10o dia de cultura). Células SCC9 expostas a culturas SAOS-2 silenciadas para OPN por RNA de interferência (RNAi) e células SCC9 cultivadas isoladamente foram usadas como controles. Após 24 h de cocultivo, células SCC9 foram avaliadas, quantitativamente, para adesão, proliferação, migração e invasão de Matrigel. A atividade de osteoclastos derivados de células monocíticas U-937 foi avaliada, quantitativamente, por meio dos ensaios de reabsorção de fosfato cálcio e de dosagem de citocinas em eluentes obtidos de células SCC9 e SAOS-2 após o cocultivo durante o pico de OPN ou com o seu silenciamento. A análise estatística foi realizada pelo teste não-paramétrico de Kruskal-Wallis (p < 0,05). Os resultados indicaram indução recíproca na expressão de OPN em SAOS-2 e SCC9 em cocultura. A OPN secretada por células SAOS-2 afetou o fenótipo de culturas SCC9, promovendo a adesão e a proliferação celulares e a invasão de Matrigel, a qual também estava aumentada, mas em menor intensidade, com o silenciamento para OPN. A migração celular não foi afetada. O cocultivo com SAOS-2, principalmente durante o pico de OPN, resultou na sobre-expressão das citocinas IL 6 e IL 8 pelas células SCC9, aumentando a capacidade de células osteoclásticas em reabsorver fosfato de cálcio. Conjuntamente, esses resultados sugerem que a OPN derivada de osteoblastos afeta as interações entre células epiteliais neoplásicas malignas, osteoblastos e osteoclastos, possivelmente contribuindo para a progressão de lesões ósseas do CEC oral
Abstract: The oral squamous cell carcinoma (OSCC) is the most prevalent malignant neoplasm of the oral structures. It may invade bone in up to 56% of the cases and promote osteoclast-mediated bone extracellular matrix (ECM) resorption. Expression of the matricellular protein osteopontin (OPN) in malignant neoplasms, including OSCC, has been positively correlated with aggressive tumor behavior. OPN is the most abundant non collagenous ECM protein in bone, where it preferentially accumulates at interfaces, including cement lines, laminae limitantes and reversal lines, being essential for the adhesion and function of osteoblasts and osteoclasts. Despite the importance attributed to OPN in the tumor microenvironment, indicative of more aggressive neoplastic phenotypes, the effects of osteoblast-derived OPN on OSCC cells and on OSCC-induced osteoclast activity are still not fully understood. The present in vitro study aimed to evaluate temporal expression of OPN in cocultures of human osteoblastic cells and malignant neoplastic epithelial cells and the effects of osteoblast-derived OPN on the neoplastic cell phenotype. Additionally, the effects of cocultures on osteoclastic activity were evaluated. Human OSCC-derived epithelial cells (SCC9 cell line) were plated on Transwell® membranes coated or not by a thin uniform layer of Matrigel and cocultured with human osteoblastic cells (SAOS-2 cell line) during its peak of OPN expression (day 10 of SAOS-2 culture). SCC9 cells exposed to OPN-silenced SAOS-2 cultures by means of interference RNA and SCC9 cells cultured alone were used as controls. At 24 h of coculture, SCC9 cells were quantitatively evaluated for cell adhesion, proliferation, migration and invasion of Matrigel. The impact of coculturing SCC9 and SAOS-2 cells either during the OPN peak expression or under the silencing of OPN was quantitatively evaluated in terms of calcium phosphate resorption by U-937-derived osteoclastic cells and expression of cytokines in the culture medium by ELISA assay. The statistical analyses were carried out using the non-parametric Kruskal-Wallis test (p < 0.05). The results showed a reciprocal induction of SAOS-2 and SCC9 cells in terms of OPN expression over the coculture interval. SAOS-2-secreted OPN altered the SCC9 cell phenotype, leading to enhanced cell adhesion and proliferation and higher Matrigel invasion, which was also enhanced, but to a lesser degree, by SAOS-2 cultures silenced for OPN. Cell migration was not affected. Cocultures with SAOS-2, mainly during the peak expression of OPN, resulted in overexpression of IL 6 and IL 8 by SCC9 cells, which corresponded with an enhanced resorptive capacity of osteoclastic cells. Taken together, the results suggest that osteoblast-derived OPN affects the interactions among malignant neoplastic epithelial cells, osteoblasts and osteoclasts, likely contributing to the progression of bone lesions in OSCC
Doutorado
Patologia
Doutor em Estomatopatologia
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Marques, Erika Afonso Costa Cortez. "Estudo da expressão e participação de osteopontina durante a interação taquizoíto de Toxoplasma gondii célula hospedeira." Universidade do Estado do Rio de Janeiro, 2007. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=2266.

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Toxoplasma gondii é um parasito do filo Apicomplexa que infecta uma grande variedade de hospedeiros, incluindo os humanos. O parasito invade a célula hospedeira por penetração ativa, com a participação das proteínas de suas organelas secretoras durante esse processo. Até o momento, somente um número limitado de proteínas secretoras tem sido descoberto, além disso, as moléculas efetoras envolvidas na invasão e sobrevivência do parasito não estão completamente compreendidas. A osteopontina (OPN) é uma glicofosfoproteína adesiva secretada, multifuncional, que contém o domínio arginina-glicina-ácido aspártico (RGD) de ligação à integrina, que está envolvida em uma variedade de eventos fisiológicos e patológicos, incluindo sinalização e sobrevivência celular. Pela primeira vez, nós demonstramos pelas técnicas de imunofluorescência e imunocitoquímica ultraestrutural que há uma intensa marcação para uma proteína OPN-like nos grânulos densos de taquizoítos de T. gondii extracelulares. O western blotting e o RT-PRC confirmaram a expressão de OPN-like nos taquizoítos. Nossos resultados também mostram que após a invasão dos macrófagos, a proteína OPN-like está localizada na membrana do vacúolo parasitóforo. Esses dados sugerem que os grânulos densos secretam uma proteína OPN-like, e nós podemos especular que essa proteína participa durante o processo de interação do parasito com as células hospedeiras. .
Toxoplasma gondii is an apicomplexan parasite infecting a broad host range, including humans. The parasite invades host cell by active penetration with the participation of its secretory organelles proteins during this process. Until now, only a limited number of secretory proteins have been discovered, and the effectors molecules involved in parasite invasion and survival are not well understood. Osteopontin (OPN) is a multifunctional secreted adhesive glycophosphoprotein containing the arginine-glycine-aspartic acid (RGD) integrin-binding domain, which is involved in various physiological and pathological events including cell signaling and survival. For the first time we demonstrated by immunofluorescence and immunoelectron microscopy approaches that there is an intense labeling for an OPN-like protein in the dense granules of extracellular T. gondii tachyzoites. Western blotting and RTPCR confirmed this protein expression in tachyzoites. Our results also showed that after macrophage invasion the OPN-like protein is localized at the parasitophorous vacuole membrane. These data suggest that dense granules secrete an OPN-like protein, and we can speculate that this protein participates during the parasite interaction process with host cells.
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Rothbarth, Claudia Pires. "Efeito do alendronato de sódio em molares de rato em formação após luxação lateral." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/23/23140/tde-19122013-153054/.

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Os bisfosfonatos são drogas capazes de inibir a reabsorção óssea por meio de seu efeito direto sobre as células ósseas, interferindo na dinâmica dos tecidos mineralizados. O alendronato (ALN), um tipo de bisfosfonato nitrogenado, foi utilizado com o objetivo de investigar os seus efeitos sobre os tecidos dentários e periodontais após luxação lateral de molares com as raízes em desenvolvimento. Ratos Wistar com 21 dias de idade tiveram os segundos molares superiores luxados lateralmente. Doses diárias de 2,5 mg / kg de ALN começaram no dia seguinte à luxação; os controles receberam solução salina estéril. As maxilas foram fixadas, descalcificadas e incluídas em parafina ou em resina Spurr 7, 14 e 21 dias pós-luxação. Os cortes foram corados com H & E, incubados por histoquímica TRAP e imuno marcados para osteopontina (OPN), bem como para análise ultraestrutural. Após 21 dias, o ápice dos molares luxados sem ALN estava aberto e desorganizado, coberto por uma camada irregular de cemento celular. Os molares luxados dos animais tratados com ALN apresentaram alguns locais de anquilose, bem como lacunas de reabsorção na superfície do cemento. Os osteoclastos TRAP positivos foram mais numerosos no grupo ALN, apesar de sua aparência latente e sua localização, afastados das trabéculas ósseas, em relação aos controles, achado que foi confirmado com a análise ultraestrutural. A imunomarcação de OPN revelou uma linha grossa imunopositiva na dentina, que deve ter surgido a partir do momento da luxação, enquanto que as amostras tratadas com ALN não apresentaram alterações na dentina. Os resultados indicam que o alendronato inibe algumas alterações na dentina e na formação do cemento, induzidas pelo trauma dental de luxação.
Bisphosphonates are drugs that inhibit bone resorption through its direct effect on bone cells, interfering with the dynamics of mineralized tissues. Alendronate (ALN), a nitrogenated bisphosphonate, was used in order to investigate their effects on dental and periodontal tissues after lateral dislocation of molars with developing roots. Twenty one days old Wistar rats had their second molars laterally l. Daily doses of 2.5 mg / kg ALN started the day following the dislocation, while controls received saline solution. The maxillae were fixed, decalcified and embedded in paraffin or in Spurr resin after 7, 14 and 21 days post-dislocation. The sections were stained with H & E, incubated for TRAP, immunolabeled for osteopontin (OPN), and ultrastructurally analyzed by transmission electron microscopy. After 21 days, the apex of the luxated molar without ALN was open and disorganized, covered by an irregular layer of cellular cementum. The luxated molar from ALN-treated animals showed some areas of ankylosis and resorption lacunae on the cementum surface. TRAP-positive osteoclasts were more numerous in the ALN group, despite their latent appearance compared to controls, a finding that was ultrastructurally confirmed. OPN immunostaining revealed a thick immunopositive line in dentin, which must be resultant from the moment of dislocation, while the samples treated with ALN showed no changes in dentin. The results indicate that alendronate inhibits some changes in dentin and cementum formation induced by dental trauma of lateral luxation.
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Smith, Laura Lee. "Osteopontin structure and function /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/6322.

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Barbosa, Ana Claudia da Silva. "Estudo das proteínas ósseas não colágenas no processo de reparação óssea alveolar em ratos idosos." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/10/10132/tde-21112013-103224/.

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O trabalho teve como objetivo avaliar e quantificar o tecido ósseo neoformado, a distribuição e a importância das proteínas não colágenas (osteocalcina, osteopontina e osteonectina) no processo de reparação tecidual do alvéolo dental de ratos Wistar idosos após exodontia. Para sua realização, foram utilizados 80 Rattus Norvegicus albinus, linhagem Wistar, machos. Os animais foram distribuídos em dois grupos: Grupo Controle, correspondente a animais com 60 dias de vida; e Grupo Experimental correspondente aos animais com 2 anos de vida (700 dias em média). Cada grupo foi dividido em 4 subgrupos de 10 animais em cada grupo. Os animais foram submetidos à exodontia do incisivo superior direito e foram sacrificados com 05, 15, 21 e 28 dias de pós-operatório. Após a dissecção, 5 amostras foram submetidas à análise por microscopia convencional com coloração por Hematoxilina e Eosina e análise da imunohistoquímica e 5 amostras para análise por RT-PCR. Os resultados mostraram que o processo de envelhecimento não alterou a cronologia do reparo ósseo alveolar e não promoveu maior remodelação do alvéolo dental. A osteocalcina não apresentou atuação importante nos períodos pós-operatórios estudados. A osteonectina apresentou-se importante no processo de reparo, não sofrendo alterações no início da reparação óssea, apresentando marcação mais intensa durante a maturação óssea entre 21 e 28 dias de pós-operatório no grupo controle e diminuição da marcação no grupo experimental aos 28 dias de pósoperatório. O envelhecimento proporcionou uma diminuição da imunomarcação da osteonectina e demonstrou marcações positivas principalmente em osteoblastos e matriz mineralizada. A osteopontina apresentou-se importante no processo de reparo ósseo durante todos os períodos pós-operatório, apresentando marcações em osteoblastos, matriz osteóide, osteócitos e matriz mineralizada, apresentando maior marcação dos tipos celulares do no grupo experimental aos 28 de pós-operatório. Apesar desses achados, novos estudos são necessários para o melhor entendimento do processo de reparo ósseo alveolar em ratos adultos e idosos.
The aim of the present study was to evaluate and quantify the newly formed bone tissue, as well as the distribution and the importance of non-collagen proteins (osteocalcin, osteopontin and osteonectin) in the process of dental alveolar repair in Wistar aged rats submitted to tooth extraction. To perform that, about 80 male Rattus Norvegicus albinus, Wistar strain, were randomly distributed into two groups: Control Group corresponding to 60 days old rats; and Experimental Group corresponding to 2 years old animals (about 700 days old). Both groups were later subdivided into 4 subgroups consisting of 10 animals each. All animals were submitted to the upright incisive tooth extraction and were euthanized 05, 15, 21 and 28 days after the tooth extraction surgery. After the dissection, five samples from each subgroup underwent conventional microscopy analysis by hematoxylin-eosin stain as well as immunohistochemistry. Bone tissue from other five samples of each groups were subjected to Real Time RT-PCR analysis of non-collagen proteins expression The results obtained suggest that aging process was not able to change either the chronology of alveolar bone repair or the remodeling of dental alveolus. Osteocalcin did not present any important action in the post-operation periods evaluated. On the other hand, osteonectin showed an important role during the repair process, since its expression was increased in the control group and decreased in comparison to the experimental group at 28 days. Osteopontin was important in the bone repair in all times evaluated, since it was present in osteoblasts, osteiod matrix, osteocytes and mineralized matrix, being even more stained at 21 days after the surgery. Finally, besides the results obtained in the present work, other studies are necessary to better understand the alveolar bone repair in adult and aged rats.
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Leitão, Glauber Moreira. "Osteopontina como marcador de resposta à radioterapia e quimioterapia em pacientes com câncer de cabeça e pescoço localmente avançado." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5155/tde-12012009-162533/.

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INTRODUÇÃO: Osteopontina (OPN) é uma glicoproteína presente em tecidos e fluidos orgânicos e envolvida em vários processos patológicos que incluem inflamação, proliferação celular, invasão da matriz extracelular, progressão tumoral e metástase. Em pacientes (pts) portadores de carcinoma epidermóide de cabeça e pescoço (CECCP), OPN tem sido associada a uma maior agressividade tumoral e empregada como marcador prognóstico. Nós investigamos o valor prognóstico e preditivo da OPN sérica em pacientes portadores de CECCP tratados de forma uniforme. MÉTODOS: Estudo longitudinal prospectivo de 47 pts portadores de CECCP localmente avançado e irressecável submetidos à quimioterapia e radioterapia. OPN sérica foi determinada pelo método ELISA (kit 1 com17 pts e kit 2 com 30 pts) com coleta realizada antes e após o término do tratamento e estudada a relação entre OPN, categorizada como alta ou baixa em relação ao valor mediano, e as características clínico-patológicas, resposta ao tratamento, sobrevida global (SG) e sobrevida livre de progressão (SLP). RESULTADOS: A OPN sérica mediana dos pacientes determinada pelo kit 1 (em ng/ml) foi de 2,1 e 1,9 pré e pós-tratamento, respectivamente; no kit 2 (em ng/ml) foi de 69,5 e 87,9 pré e pós-tratamento, respectivamente. Pacientes portadores de tumores de orofaringe foram mais freqüentemente associados a baixos níveis séricos de OPN pós-tratamento, em comparação com outros sub-sítios (p=0,03). Observada tendência à associação entre os valores séricos baixos de osteopontina pós-tratamento e a resposta tratamento (p=0,06). Houve associação entre os valores elevados da osteopontina pós-tratamento e menor SLP (p=0,09, log rank), com medianas de 11,9 meses e 14,5 meses, conforme valores séricos de OPN pós-tratamento altos e baixos, respectivamente. Não houve associação dos valores séricos de OPN pré e pós-tratamento e a SG (p=0,19 e p= 0,10, respectivamente). CONCLUSÃO: Neste grupo de pacientes portadores de CECCP, sugere-se que OPN sérica baixa após a quimioradioterapia associa-se à resposta ao tratamento e melhor SLP.
INTRODUCTION: Osteopontin (OPN) is a glycoprotein present in tissues and body fluids involved in several pathological processes that include inflammation, cell proliferation, invasion of the extracellular matrix, tumor progression and metastasis. In head and neck squamous cell carcinoma (HNSCC) patients, OPN has been associated with greater tumor aggressiveness and used as a prognostic marker. We investigated the prognostic and predictive value of plasma OPN in homogeneously treated (HNSCC) patients. METHODS: Longitudinal prospective study of 47 patients with locally advanced and inoperable HNSCC treated with exclusive platin based concomitant chemoradiotherapy. Plasma OPN was determined by ELISA (n=14 kit I, n=32 kit II) pre and postreatment and correlated with tumor response, overall survival (OS) and progression-free survival (PFS). RESULTS: Median OPN levels in ng/ml were 2,1 and 1,9 pre and postreatment, respectively, by kit I and 69,5 and 87,9 by kit II. Patients were categorized as OPN low or high, using the median as a cut-off point. Patients with oropharynx tumors, as compared to other subsites, were more frequently categorized as low OPN (p = 0,03). A low postreatment OPN level was associated with tumor response (p = 0,06) and a high postreatment OPN level was associated with poor PFS, 11.9 vs. 14.5 months (p=0.09, log rank). Mean OS was 16.2 and 13.7 months in low and high postreatment OPN pts, respectively (p=0.10, log rank). CONCLUSIONS: In this group of HNSCC patients, it is suggested that a low plasma OPN after chemoradiotherapy is associated with a lower response rate and a worse PFS.
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Pereira, Thiago de Almeida. "Participação da via do Hedgehog na fibrose hepática da esquistossomose mansoni humana e murina experimental." reponame:Repositório Institucional da FIOCRUZ, 2015. https://www.arca.fiocruz.br/handle/icict/14002.

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Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
INTRODUÇÃO/OBJETIVO: A esquistossomose mansonica é causa importante de fibrose hepática e hipertensão porta em regiões tropicais, e a patogênese da fibrose não está bem esclarecida. Como a via do hedgehog e um dos seus genes alvos, a osteopontina, estão envolvidos em fibroses hepáticas de outras etiologias o objetivo foi investigar a ativação destas vias na esquIsitossomose humana e murina experimental, no intuito de verificar o seu envolvimento no desenvolvimento da forma hepatoesplênica da esquistossomose mansonica (FHE). MATERIAL E MÉTODOS: 87 biópsias em cunha de fígados de pacientes com FHE submetidos a cirurgia e fragmentos de fígado de camundongos suiços infectados com Schistosoma mansoni foram submetidos a métodos imunohistoquímicos e de biologia molecular para avaliar a expressão de ligantes hedgehog (Ihh, Shh), receptor Patched, fatores de transcrição Gli 1 e 2 e osteopontina. Osteopontina sérica e ligante Shh do hedgehog foram avaliados em camundongos suíços infectados e os de osteopontina em camundongos CBA/J infectados e em pacientes com FHE e forma hepatointestinal da esquistossomose. In vitro foi avaliado o efeito de antígeno solúvel do ovo (SEA) em células de Kuppfer, células estreladas, macrófagos, colangiócitos e células endoteliais sinusoidais hepáticas. A relação com a via da IL-13 foi avaliada em camundongos geneticamente deficientes ou hiperexpressando a citocina. Foi avaliado in vitro se a IL-13 induz ligantes hedghog ou ativação da via em células de Kuppfer. RESULTADOS: Os resultados mostraram: (a) aumento expressão de ligantes Ihh, de fatores de transcrição Gli2 e de osteopontina no fígado de camundongos suíços infectados com Schistosoma mansoni, aumento de shh e osteopontina no plasma de camundongos suíços e de osteopontina no plasma de camundongos CBA/J infectados com S. mansoni; (b) aumento na expressão de Ihh, Shh, Gli1 e 2, receptor Patched e de osteopontina no fígado de pacientes com esquistossomose e aumento da osteopontina sérica em pacientes com a FHE; (c) A expressão de ligantes hedgehog e de Gli2 foi observada em macrófagos, células estreladas, ductos biliares e células endoteliais, e a de osteoponina em ductos biliares, macrófagos e células estreladas/miofibroblastos; (d) correlação positiva entre ativação do hedgehog (Gli2 e osteopontina) e fibrose, no modelo murino experimental e nos pacientes; nestes a correlação também foi observada com o grau de fibrose classificada pelo ultrassom e com a hipertensão porta; (e) Inibição in vitro do hedgehog com ciclopamina e vismodegib ou por nocauteamento condicional de receptor Smoothened bloqueou a ativação alternativa de macrófagos e inibiu a angiogênese a partir de células endoteliais sinusoidais hepáticas; (f) que o bloqueio da via da IL-13 reduziu e a hiperexpressão aumentou a ativação da via do hedgehog e IL-13 diretamente induziu, in vitro, produção de ihh em células de Kupffer de camundongos e de humanos, demonstrando a inter-relação das duas vias. CONCLUSÃO: Pode-se concluir que a via do hedgehog tem participação importante na patogênese da fibrose hepática esquistossomótica, atuando através de estímulos à fibrogênese e à angiogênese e que a osteopontina é candidata a ser um biomarcador de intensidade da fibrose e da hipertensão porta na doença.
BACKGROUND AND AIMS: Schistosomiasis is a major cause of liver fibrosis and portal hypertension in tropical regions, and the pathogenesis of fibrosis is not well established. As hedgehog pathway and one of its target genes, osteopontin, are involved in liver fibrosis of other etiologies our aims were to investigate the activation of these pathways in human and experimental murine schistosomiasis, in an attempt to verify their involvement in the development of hepatosplenic schistosomiasis mansoni (HS). METHODS: 87 wedge liver biopsies of patients with HS submitted to surgery and liver fragments Swiss mice infected with Schistosoma mansoni were submitted to immunohistochemistry and molecular biology methods to evaluate the expression of hedgehog ligands (Ihh, Shh), patched receptor , Gli transcription factors and osteopontin. Serum osteopontin and Shh were evaluated in infected Swiss mice and osteopontin was evaluated in serum of infected CBA/J mice and plasma from patients with hepatointestinal and HS forms of schistosomiasis. The effect of soluble egg antigen (SEA) on Kuppfer cells, stellate cells, macrophages, cholangiocytes and liver sinusoidal endothelial cells was evaluated in vitro. Relationship with IL-13 pathway was evaluated in mice genetically deficient or with hyperexpression of this cytokine. Whether IL-13 induces production of ligands and/or activation of the hedgehog pathway in Kuppfer cells was evaluated in vitro. RESULTS: Results demonstrated: (a) increased expression of Ihh, transcription factor Gli2 and osteopontin in the livers of Swiss mice infected with S. mansoni, increased plasma levels of shh and osteopontin in infected Swiss mice and increased osteopontin in plasma of S. mansoni infected CBA/J mice; (b) increased expression of ihh, shh, Gli1 and 2, patched and osteopontin receptor in the liver of patients with schistosomiasis and increased serum osteopontin in patients with HS; (c) expression of hedgehog ligands and Gli2 was observed in macrophages, stellate cells, endothelial cells and bile duct and expression of osteopontin was detected in macrophages and stellate/myofibroblast cells; (d) positive correlation between activation of the hedgehog (Gli2 and osteopontin) and fibrosis in experimental murine model and in patients; these correlation was also observed with the degree of fibrosis classified by ultrasound and with portal hypertension; (e) in vitro inhibition of hedgehog pathway with cyclopamine or vismogedib or by conditional knockout of Smoothened co-receptor blocked the alternative activation of macrophage and inhibited angiogenesis in liver sinusoidal endothelial cells; (f) reduction of IL-13 pathway or IL-13 over-expression respectively reduced or increased the activation of the hedgehog pathway and IL-13 directly induced in vitro ihh production in Kupffer cells from mice and human, demonstrating a cross-talk between the two pathways. CONCLUSION: In conclusion the hedgehog pathway plays an important role in the pathogenesis of liver fibrosis in schistosomiasis mansoni, acting through stimulation of angiogenesis and fibrogenesis and osteopontin is a putative candidate to be a biomarker of intensity of fibrosis and portal hypertension in the disease.
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Myers, Daniel. "The Role of Osteopontin in Vascular Remodeling." Fogler Library, University of Maine, 2004. http://www.library.umaine.edu/theses/pdf/MyersDL2004.pdf.

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Books on the topic "Osteopontiini"

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Zohar, Ron. Intracellular osteopontin: Relationship to osteogenic differentiation and cell migration. [Toronto: University of Toronto, Faculty of Dentistry], 1998.

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Guo, Peirong. Immuno-scanning electron microscopy localization of osteopontin at remodelling sites in rat femora. Ottawa: National Library of Canada, 1996.

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Guo, Peirong. Immune-scanning electron microscopy localization of osteopontin at remodelling sites in rat femora. [Toronto: University of Toronto], 1996.

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T, Denhardt David, ed. Osteopontin: Role in cell signalling and adhesion. New York, N.Y: New York Academy of Sciences, 1995.

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Zhu, Baoqian. Characterization of a novel intracellular form of osteopontin. 2002, 2002.

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Cogan, Gabrielle. Expression of bone sialoprotein and osteopontin in breast cancer. 2002 [i.e. 2003], 2003.

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Denhardt, David T. Osteopontin: Role in Cell Signalling and Adhesion (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1995.

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Butler, William T. Osteopontin: Role in Cell Signalling and Adhesion (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1995.

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Zhang, Qi. Isolation and characterization of porcine bone sialoproteins and the study of osteopontin (bone sialoprotein I) gene regulation. 1993.

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Ali-Fehmi, Rouba, and Eman Abdulfatah. Biological Aspects and Clinical Applications of Serum Biomarkers in Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0002.

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Ovarian cancer, the most aggressive gynecological malignancy, presents at advanced stages with metastatic disease. Diagnosis at an early stage is the most important determinant of survival; however, the majority of patients are asymptomatic at early stages and the current diagnostic tools used in clinics show limited success in early detection and hence the need for new diagnostic biomarkers. With the advance of techniques in genomic and proteomics, numerous biomarkers are emerging which may serve as a platform for early detection of ovarian cancer. These include gene-, protein-, miRNAs, and metabolite- based biomarkers. Examples of gene-based biomarkers include HE4, FLOR1, p16INK4a, BRCA1, BRCA2, MLH1, and MSH2. Protein- based biomarkers include leptin, prolactin, osteopontin, IGF-II, and MIF. This chapter discusses the serum tumor markers (CA-125) in current use for screening, diagnosis and monitoring of ovarian cancer as well as the novel biomarkers that are under investigation and validation.
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Book chapters on the topic "Osteopontiini"

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Allan, Alison L. "Osteopontin." In Encyclopedia of Cancer, 2664–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4286.

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Holdenrieder, S. "Osteopontin." In Springer Reference Medizin, 1800. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_2322.

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Holdenrieder, S. "Osteopontin." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_2322-1.

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Allan, Alison L. "Osteopontin." In Encyclopedia of Cancer, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_4286-5.

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Allan, Alison L. "Osteopontin." In Encyclopedia of Cancer, 3252–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_4286.

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Bawage, Swapnil, Shannon E. Weeks, Lalita A. Shevde, and Rajeev S. Samant. "Osteopontin (Spp1)." In Encyclopedia of Signaling Molecules, 3677–86. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101771.

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Bawage, Swapnil, Shannon E. Weeks, Lalita A. Shevade, and Rajeev S. Samant. "Osteopontin (Spp1)." In Encyclopedia of Signaling Molecules, 1–10. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101771-1.

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Graf, Kristof. "Osteopontin in Kardiomyozyten." In Bedeutung der Zell-Matrix-Interaktion für die linksventrikuläre Hypertrophie, 35–39. Heidelberg: Steinkopff, 2000. http://dx.doi.org/10.1007/978-3-642-93713-2_6.

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Graf, Kristof. "Osteopontin im menschlichen Herzen." In Bedeutung der Zell-Matrix-Interaktion für die linksventrikuläre Hypertrophie, 49–54. Heidelberg: Steinkopff, 2000. http://dx.doi.org/10.1007/978-3-642-93713-2_8.

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Graf, Kristof. "Osteopontin und linksventrikuläre Hypertrophie (Tiermodell)." In Bedeutung der Zell-Matrix-Interaktion für die linksventrikuläre Hypertrophie, 40–48. Heidelberg: Steinkopff, 2000. http://dx.doi.org/10.1007/978-3-642-93713-2_7.

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Conference papers on the topic "Osteopontiini"

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Sorensen, Esben S. "STRUCTURAL STUDIES ON OSTEOPONTIN." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.273.

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Noda, Masaki. "OSTEOPONTIN FUNCTION IN BONE." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.332.

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Boskey, Adele L. "OSTEOPONTIN AND BIOMINERALIZATON: AN OVERVIEW." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.251.

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Zohar, Ron, Baoqian Zhu, Christopher A. G. McCulloch, and Jaro Sodek. "INTRACELLULAR OSTEOPONTIN AND CELL SURVIVAL." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.268.

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Singh, Krishna. "OSTEOPONTIN: ROLE IN MYOCARDIAL REMODELING." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.274.

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Tilli, Tatiana M., Kivvi Duarte De Mello, Maria Theresa Accioly, Paulo Antonio Faria, and Etel Rp Gimba. "Abstract 89: Osteopontin-c and osteopontin-b splicing isoforms activate prostate cancer progression features." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-89.

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Hampel, Dierk J., Victor I. Romanov, Susan R. Rittling, David T. Denhardt, and Michael S. Goligorsky. "MODE OF OSTEOPONTIN ACTION AS A SURVIVAL FACTOR: STUDY OF OSTEOPONTIN-DEFICIENT 3T3 FIBROBLASTS." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.301.

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Mello, Kivvi Duarte, Tatiana Martins Tilli, Ana Carolina S. Ferreira, Claudete Esteves Klumb, Luiz Eurico Nasciutti, and Etel Rodrigues Pereira Gimba. "Abstract 1346: Osteopontin-b and Osteopontin-c splicing isofoms activate prostate cancer cells prosurvival features." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1346.

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Rittling, Susan R., Brenda Bourassa, and Yanping Chen. "ROLE OF HOST OSTEOPONTIN IN TUMORIGENESIS." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.248.

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Kaartinen, Mari T., Sherif El-Maadawy, Niina H. Rasanen, Pekka H. Maenpaa, Janet Moradian-Oldak, and Marc D. McKee. "OSTEOPONTIN AS A SUBSTRATE FOR TRANSGLUTAMINASE." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.256.

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Reports on the topic "Osteopontiini"

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Karcher, Elizabeth L., Donald C. Beitz, and Judith R. Stabel. Osteopontin Expression in Periparturient Dairy Cows Naturally Infected with Mycobacterium Avium Subsp. Paratuberculosis. Ames (Iowa): Iowa State University, January 2008. http://dx.doi.org/10.31274/ans_air-180814-843.

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Weber, George F. Contribution of the Receptor/Ligand Interaction Between CD44 and Osteopontin to Formation of Breast Cancer Metastases. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada384133.

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Weber, Georg. Contribution of the Receptor/Ligand Interaction Between CD44 and Osteopontin to Formation of Breast Cancer Metastases. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada393323.

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You might also be interested in the extended bibliographies on the topic 'Osteopontiini' for particular source types:
Journal articles Dissertations / Theses
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