Relevant bibliographies by topics / Vitamin D Receptor (VDR)

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Academic literature on the topic 'Vitamin D Receptor (VDR)'

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

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Journal articles on the topic "Vitamin D Receptor (VDR)"

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Sánchez-Martínez, Ruth, Alberto Zambrano, Ana I. Castillo, and Ana Aranda. "Vitamin D-Dependent Recruitment of Corepressors to Vitamin D/Retinoid X Receptor Heterodimers." Molecular and Cellular Biology 28, no. 11 (March 24, 2008): 3817–29. http://dx.doi.org/10.1128/mcb.01909-07.

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ABSTRACT Transcriptional regulation by nuclear receptors is mediated by recruitment of coactivators and corepressors. In the classical model, unliganded nonsteroidal receptors bind corepressors, such as the silencing mediator of thyroid and retinoid receptors (SMRT) or nuclear corepressor (NCoR), that are released upon ligand binding. We show here that, unlike other receptors, the heterodimer of the vitamin D receptor (VDR) with the retinoid X receptor (RXR) recruits NCoR and SMRT strictly in a VDR agonist-dependent manner. Binding of an agonist to VDR allows its partner receptor, RXR, to bind the corepressors. The RXR ligand has the opposite effect and induces corepressor release from the heterodimer. 1,25-Dihydroxy-vitamin D3 (VD3) causes recruitment of SMRT and NCoR to a VDR target promoter. Down-regulation of corepressors by means of small interfering RNA enhances transcriptional responses to VD3. These data reveal a new paradigm of SMRT and NCoR binding to nuclear receptors and demonstrate that these corepressors can function as physiological negative regulators of VD3-mediated transcription.
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Takeyama, Ken-Ichi, Yoshikazu Masuhiro, Hiroaki Fuse, Hideki Endoh, Akiko Murayama, Sachiko Kitanaka, Miyuki Suzawa, Junn Yanagisawa, and Shigeaki Kato. "Selective Interaction of Vitamin D Receptor with Transcriptional Coactivators by a Vitamin D Analog." Molecular and Cellular Biology 19, no. 2 (February 1, 1999): 1049–55. http://dx.doi.org/10.1128/mcb.19.2.1049.

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ABSTRACT The nuclear vitamin D receptor (VDR) is a member of a nuclear receptor superfamily and acts as a ligand-dependent transcription factor. A family of cotranscriptional activators (SRC-1, TIF2, and AIB-1) interacts with and activates the transactivation function of nuclear receptors in a ligand-dependent way. We examined interaction of VDR with these coactivators that was induced by several vitamin D analogs, since they exert differential subsets of the biological action of vitamin D through unknown mechanisms. Unlike other vitamin D analogs tested, OCT (22-oxa-1α,25-dihydroxyvitamin D3) induced interaction of VDR with TIF2 but not with SRC-1 or AIB-1. Consistent with these interactions, only TIF2 was able to potentiate the transactivation function of VDR bound to OCT. Thus, the present findings suggest that the structure of VDR is altered in a vitamin D analog-specific way, resulting in selective interactions of VDR with coactivators. Such selective interaction of coactivators with VDR may specify the array of biological actions of a vitamin D analog like OCT, possibly through activating a particular set of target gene promoters.
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Li, S. M., L. H. Ouyang, and D. G. Zhou. "Effects of vitamin D3 on expression of defensins, Toll-like receptors, and vitamin D receptor in liver, kidney, and spleen of Silky Fowl." Czech Journal of Animal Science 58, No. 1 (January 8, 2013): 1–7. http://dx.doi.org/10.17221/6519-cjas.

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The expression of avian &beta;-defensins (AvBDs), Toll-like receptors (TLRs), and vitamin D receptor (VDR) following in vivo vitamin D<sub>3 </sub>injection was studied. Healthy 90-day Silky Fowls were abdominally injected with vitamin D<sub>3</sub> or untreated. Real-time PCR analyses revealed that injection of vitamin D<sub>3</sub> significantly (P &lt; 0.05) up-regulated the expression of TLRs (TLR2, TLR5), VDR, AvBDs (AVBD-6, GAL-1), and 24-hydroxylase (CYP24A1) in the tissues (liver, spleen, and kidney) at various times 8&ndash;24 h post injection. These results suggest that expression of VDR, AvBDs, and TLRs seems to be induced by vitamin D<sub>3 </sub>and it was concluded that the tissues expressing TLRs and VDR respond to vitamin D<sub>3</sub> and in turn upregulate these tissues cellular functions to synthesize AvBDs. Intraperitoneal injection of vitamin D<sub>3</sub> likely resulted in enhancing the expression of AvBDs, TLRs, and VDR, which providedinsight into factors important for the control of the innateimmune response in the chickens.
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Takeshita, Akira, Yasunori Ozawa, and William W. Chin. "Nuclear Receptor Coactivators Facilitate Vitamin D Receptor Homodimer Action on Direct Repeat Hormone Response Elements." Endocrinology 141, no. 3 (March 1, 2000): 1281–84. http://dx.doi.org/10.1210/endo.141.3.7441.

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Abstract Vitamin D receptor (VDR) is a ligand-dependent transcription factor that regulates target gene expression. Although VDR forms stable heterodimer complex with retinoid X receptors (RXRs) on vitamin D-response elements (VDREs), it is still not clear whether VDR/RXR heterodimers are the only VDR complexes responsible for vitamin D-mediated gene transcription. In this report, we analyzed the effect of nuclear receptor coactivators (SRC-1 and TRAM-1) on VDR homodimer and VDR/RXR heterodimer formation by electrophoretic mobility shift assay. We found that VDR forms stable homodimers after interaction with the coactivators on a VDRE (DR+3). Of particular note, DR+4 and DR+5 hormone-response elements (HREs) may also support such interactions. Cotransfection experiments revealed further that the coactivators enhance ligand-induced VDR transcription on these elements. Our studies suggest the important role of VDR homodimers, in addition to VDR/RXR heterodimers, in vitamin D-induced transactivation. Thus, specific coactivator-VDR interactions on HREs may determine target gene transactivation.
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Bouillon, Roger, Geert Carmeliet, Lieve Verlinden, Evelyne van Etten, Annemieke Verstuyf, Hilary F. Luderer, Liesbet Lieben, Chantal Mathieu, and Marie Demay. "Vitamin D and Human Health: Lessons from Vitamin D Receptor Null Mice." Endocrine Reviews 29, no. 6 (October 1, 2008): 726–76. http://dx.doi.org/10.1210/er.2008-0004.

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Abstract The vitamin D endocrine system is essential for calcium and bone homeostasis. The precise mode of action and the full spectrum of activities of the vitamin D hormone, 1,25-dihydroxyvitamin D [1,25-(OH)2D], can now be better evaluated by critical analysis of mice with engineered deletion of the vitamin D receptor (VDR). Absence of a functional VDR or the key activating enzyme, 25-OHD-1α-hydroxylase (CYP27B1), in mice creates a bone and growth plate phenotype that mimics humans with the same congenital disease or severe vitamin D deficiency. The intestine is the key target for the VDR because high calcium intake, or selective VDR rescue in the intestine, restores a normal bone and growth plate phenotype. The VDR is nearly ubiquitously expressed, and almost all cells respond to 1,25-(OH)2D exposure; about 3% of the mouse or human genome is regulated, directly and/or indirectly, by the vitamin D endocrine system, suggesting a more widespread function. VDR-deficient mice, but not vitamin D- or 1α-hydroxylase-deficient mice, and man develop total alopecia, indicating that the function of the VDR and its ligand is not fully overlapping. The immune system of VDR- or vitamin D-deficient mice is grossly normal but shows increased sensitivity to autoimmune diseases such as inflammatory bowel disease or type 1 diabetes after exposure to predisposing factors. VDR-deficient mice do not have a spontaneous increase in cancer but are more prone to oncogene- or chemocarcinogen-induced tumors. They also develop high renin hypertension, cardiac hypertrophy, and increased thrombogenicity. Vitamin D deficiency in humans is associated with increased prevalence of diseases, as predicted by the VDR null phenotype. Prospective vitamin D supplementation studies with multiple noncalcemic endpoints are needed to define the benefits of an optimal vitamin D status.
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Thorne, James, and Moray J. Campbell. "The vitamin D receptor in cancer." Proceedings of the Nutrition Society 67, no. 2 (April 15, 2008): 115–27. http://dx.doi.org/10.1017/s0029665108006964.

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Over the last 25 years roles have been established for vitamin D receptor (VDR) in influencing cell proliferation and differentiation. For example, murine knock-out approaches have revealed a role for the VDR in controlling mammary gland growth and function. These actions appear widespread, as the enzymes responsible for 1α,25-dihydroxycholecalciferol generation and degradation, and the VDR itself, are all functionally present in a wide range of epithelial and haematopoietic cell types. These findings, combined with epidemiological and functional data, support the concept that local, autocrine and paracrine VDR signalling exerts control over cell-fate decisions in multiple cell types. Furthermore, the recent identification of bile acid lithocholic acid as a VDR ligand underscores the environmental sensing role for the VDR.In vitroandin vivodissection of VDR signalling in cancers (e.g. breast, prostate and colon) supports a role for targeting the VDR in either chemoprevention or chemotherapy settings. As with other potential therapeutics, it has become clear that cancer cells displayde novoand acquired genetic and epigenetic mechanisms of resistance to these actions. Consequently, a range of experimental and clinical options are being developed to bring about more targeted actions, overcome resistance and enhance the efficacy of VDR-centred therapeutics.
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Brown, Alex J., Adriana Dusso, and Eduardo Slatopolsky. "Vitamin D." American Journal of Physiology-Renal Physiology 277, no. 2 (August 1, 1999): F157—F175. http://dx.doi.org/10.1152/ajprenal.1999.277.2.f157.

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The vitamin D endocrine systems plays a critical role in calcium and phosphate homeostasis. The active form of vitamin D, 1,25-dihydroxyvitamin D3[1,25(OH)2D3], binds with high affinity to a specific cellular receptor that acts as a ligand-activated transcription factor. The activated vitamin D receptor (VDR) dimerizes with another nuclear receptor, the retinoid X receptor (RXR), and the heterodimer binds to specific DNA motifs (vitamin D response elements, VDREs) in the promoter region of target genes. This heterodimer recruits nuclear coactivators and components of the transcriptional preinitiation complex to alter the rate of gene transcription. 1,25(OH)2D3also binds to a cell-surface receptor that mediates the activation of second messenger pathways, some of which may modulate the activity of the VDR. Recent studies with VDR-ablated mice confirm that the most critical role of 1,25(OH)2D3is the activation of genes that control intestinal calcium transport. However, 1,25(OH)2D3can control the expression of many genes involved in a plethora of biological actions. Many of these nonclassic responses have suggested a number of therapeutic applications for 1,25(OH)2D3and its analogs.
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Ogbu, Destiny, Eric Xia, and Jun Sun. "Gut instincts: vitamin D/vitamin D receptor and microbiome in neurodevelopment disorders." Open Biology 10, no. 7 (July 2020): 200063. http://dx.doi.org/10.1098/rsob.200063.

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The gut microbiome regulates a relationship with the brain known as the gut–microbiota–brain (GMB) axis. This interaction is influenced by immune cells, microbial metabolites and neurotransmitters. Recent findings show gut dysbiosis is prevalent in autism spectrum disorder (ASD) as well as attention deficit hyperactivity disorder (ADHD). There are previously established negative correlations among vitamin D, vitamin D receptor (VDR) levels and severity of ASD as well as ADHD. Both vitamin D and VDR are known to regulate homeostasis in the brain and the intestinal microbiome. This review summarizes the growing relationship between vitamin D/VDR signalling and the GMB axis in ASD and ADHD. We focus on current publications and summarize the progress of GMB in neurodevelopmental disorders, describe effects and mechanisms of vitamin D/VDR in regulating the microbiome and synoptically highlight the potential applications of targeting vitamin D/VDR signalling in neurodevelopment disorders.
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Zwerina, Karin, Wolfgang Baum, Roland Axmann, Gisela Ruiz Heiland, Jörg H. Distler, Josef Smolen, Silvia Hayer, Jochen Zwerina, and Georg Schett. "Vitamin D receptor regulates TNF-mediated arthritis." Annals of the Rheumatic Diseases 70, no. 6 (March 17, 2011): 1122–29. http://dx.doi.org/10.1136/ard.2010.142331.

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ObjectiveReduced vitamin D intake has been linked to increased susceptibility to develop rheumatoid arthritis (RA) and vitamin D deficiency is associated with increased disease activity in RA patients. The pathophysiological role of vitamin D in joint inflammation is, however, unclear.MethodsTo determine the influence of absent vitamin D signalling in chronic arthritis, vitamin D receptor (VDR)-deficient mice were crossed with human tumour necrosis factor (TNF) transgenic mice (hTNFtg), which spontaneously develop chronic arthritis.ResultsClinical signs and symptoms of chronic arthritis were aggravated in hTNFtg mice lacking functional VDR signalling. Moreover, synovial inflammation was clearly increased in VDR−/−hTNFtg mice as compared to hTNFtg mice and was associated with an increased macrophage influx in inflamed joints. In vitro, VDR-deficient monocytes were proinflammatory and hyper-responsive to TNF stimulation associated with prolonged mitogen-activated protein kinase activation and cytokine secretion. Also, VDR−/− monocytes showed enhanced potential to differentiate into bone resorbing osteoclasts in vitro. In line, VDR−/−hTNFtg mice had significantly increased cartilage damage and synovial bone erosions.ConclusionsVDR plays an important role in limiting the inflammatory phenotype in a mouse model of RA. Absent VDR signalling causes a proinflammatory monocyte phenotype associated with increased inflammation, cartilage damage and bone erosion.
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Dusso, Adriana S., Alex J. Brown, and Eduardo Slatopolsky. "Vitamin D." American Journal of Physiology-Renal Physiology 289, no. 1 (July 2005): F8—F28. http://dx.doi.org/10.1152/ajprenal.00336.2004.

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The vitamin D endocrine system plays an essential role in calcium homeostasis and bone metabolism, but research during the past two decades has revealed a diverse range of biological actions that include induction of cell differentiation, inhibition of cell growth, immunomodulation, and control of other hormonal systems. Vitamin D itself is a prohormone that is metabolically converted to the active metabolite, 1,25-dihydroxyvitamin D [1,25(OH)2D]. This vitamin D hormone activates its cellular receptor (vitamin D receptor or VDR), which alters the transcription rates of target genes responsible for the biological responses. This review focuses on several recent developments that extend our understanding of the complexities of vitamin D metabolism and actions: the final step in the activation of vitamin D, conversion of 25-hydroxyvitamin D to 1,25(OH)2D in renal proximal tubules, is now known to involve facilitated uptake and intracellular delivery of the precursor to 1α-hydroxylase. Emerging evidence using mice lacking the VDR and/or 1α-hydroxylase indicates both 1,25(OH)2D3-dependent and -independent actions of the VDR as well as VDR-dependent and -independent actions of 1,25(OH)2D3. Thus the vitamin D system may involve more than a single receptor and ligand. The presence of 1α-hydroxylase in many target cells indicates autocrine/paracrine functions for 1,25(OH)2D3in the control of cell proliferation and differentiation. This local production of 1,25(OH)2D3is dependent on circulating precursor levels, providing a potential explanation for the association of vitamin D deficiency with various cancers and autoimmune diseases.
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Dissertations / Theses on the topic "Vitamin D Receptor (VDR)"

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Hill, Natasha Tremayne. "Vitamin D receptor and 1alpha, 25-dihydroxyvitamin D3 mediated regulation of DeltaNp63alpha." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1450456950.

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Xavier, David André Rodrigues. "Vitamin D receptor (VDR) gene polymorphisms and genetic susceptibility to thyroid cancer." Master's thesis, Universidade da Beira Interior, 2013. http://hdl.handle.net/10400.6/1630.

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Thyroid cancer is the most common endocrine malignancy and a complex disease with a largely unknown aetiology. Thyroid carcinomas are derived from thyroid follicular cells and parafollicular cells. The majority of thyroid cancer cases comprise both papillary (PTC) and follicular carcinomas (FTC). The evaluation of genetic susceptibility could give valuable information regarding the risk of thyroid cancer development. There are many genes associated with the thyroid function that modulates the risk of tumour development. Among them, is the vitamin D receptor gene (VDR), located on chromosome 12q12-q14, and includes eight protein coding exons (exons 2-9) and one untranslated exon (exons 1a-1f). The most common VDR polymorphisms investigated are FokI (rs10735810 C>T), located in exon 2 of VDR, BsmI (rs1544410 G>A) and ApaI (rs7975232 G>T), located in intron 8, and TaqI (rs731236 T>C), located in exon 9 of VDR. The importance of vitamin D and its receptor VDR, in many signalling pathways is well known. Therefore we aim to verify in which way VDR polymorphisms influence the predisposition for thyroid cancer development. The contribution of four well-known VDR polymorphisms (FokI, BsmI, ApaI and TaqI) for the genetic susceptibility of thyroid cancer in the Portuguese population was analysed, including haplotypes comparisons. The following parameters were studied: thyroid cancer type differences (PTC vs. FTC), age (≤45 vs. >45 years), gender (male vs. female), carcinoma size (≤10mm vs. >10mm), lymph node metastasis and distant metastasis multicentricity, and stage of cancer (I-II vs. III-IV). All the participants in the study were Caucasian Portuguese inhabitants, being subdivided into two groups: patients with thyroid cancer (N = 208) and a control group (N = 248). In conclusion, there were some statistically significant differences in some parameters assessed. However, the results considered were only those with a statistical significant p-value < 0.005, according to Bonferroni’s correction. Therefore, the results suggest that BsmI polymorphism genotype AA (p = 0.004) may influence lymph node metastasis or distant metastasis in patients with DTC. Moreover, the TT genotype (p = 0.004) of ApaI polymorphism may increase the predisposition for more aggressive phenotypes of DTC, since it is overrepresented in patients with more advanced cancer stages (III-IV).
O cancro da tiróide é, de todas as neoplasias endócrinas, a mais comum, revelando ser uma patologia complexa e com uma etiologia desconhecida em parte. Tem uma incidência mundial que tem tendência a aumentar, contabilizando cerca de 1.7% dos cancros diagnosticados. Adicionalmente, o cancro da tiróide é mais prevalente em pacientes de meia idade e idosos, onde mais de metade dos indivíduos diagnosticados têm uma idade superior aos 45 anos. Ademais, esta neoplasia endócrina é mais comum nas mulheres, com uma incidência de 3 a 5 vezes maior. Os nódulos que surgem na tiróide são diagnosticados em cerca de 5% da população adulta mundial, e podem ser adenomas ou lesões malignas. Os carcinomas da tiróide derivam quer das células foliculares da tiróide, bem como das células C, porém, a grande maioria deles tem origem nas células foliculares. De todas as variantes de carcinomas da tiróide, os carcinomas papilar e folicular da tiróide são os mais predominantes, sendo a variante papilar a mais comum de entre todos, seguida da variante folicular. Apesar da elevada incidência mundial de cancro da tiróide, a taxa de mortalidade associada permanece estável. O tratamento do cancro da tiróide é um processo multifatorial, envolvendo a combinação de terapias cirúrgicas, hormonais ou de medicina nuclear. Sabe-se que o cancro da tiróide, em especial os tumores diferenciados da tiróide, estão a aumentar de incidência em alguns países desenvolvidos. Existem muitos fatores de risco que aumentam a predisposição para este tipo de cancro, incluindo fatores genéticos com risco associado a esta patologia. A título de exemplo, o cancro diferenciado da tiróide está associado a uma forte hereditariedade, aumentando a suscetibilidade genética do indivíduo em desenvolver cancro de acordo com o seu historial familiar. Para além disso, a presença de polimorfismos genéticos podem determinar a suscetibilidade individual do indivíduo para o desenvolvimento de cancro da tiróide. Atualmente são conhecidos vários genes associados com a função tiroideia e que modulam o risco para a tumorigénese. O VDR é um membro da superfamília de recetores nucleares, sendo a única proteína com afinidade para a 1α,25-dihidroxivitamina D, também conhecida como calcitriol. Nos mamíferos, a expressão do VDR encontra-se aumentada em tecidos metabólicos tais como o intestino, rins, pele e glândula da tiróide. O impacto biológico do VDR surge quando este se liga aos seus elementos localizados nas regiões promotores dos genes alvo, interferindo assim em muitas ações celulares e moleculares que vão desde a regulação do metabolismo de cálcio até à regulação de péptidos antimicrobiais. Desta forma, a ação molecular da vitamina D/ VDR está envolvida na regulação mineral e homeostase óssea, modulação do crescimento, eventos cardiovasculares, prevenção de cancro e regulação de respostas imunes. Uma disfunção do VDR ou défice de vitamina D podem levar a consequências no desenvolvimento e saúde óssea assim como aumentar a predisposição do indivíduo para o desenvolvimento de algumas doenças crónicas, incluindo o cancro. Os polimorfismos associados ao gene VDR já provaram estar implicados como um fator principal de risco em vários tipos de cancro, tais como o cancro da próstata, mama ou cólon. Ao longo do tempo, estudos de associação têm sido feitos de modo a se poder correlacionar os polimorfismos genéticos e o seu impacto na saúde do indivíduo. Assim, no presente trabalho pretende-se estudar a suscetibilidade genética do cancro da tiróide associada aos polimorfismos do gene VDR. Neste trabalho, foram estudados quatro polimorfismos diferentes gene do VDR. Para tal, através do uso de enzimas de restrição, foi possível analisar áreas restritas do gene VDR, localizado no cromossoma 12q12-q14 de forma a se poder observar variações da sequência de DNA. Os quatro polimorfismos estudados no âmbito deste projeto foram o FokI (rs10735810 C>T), localizado no exão 2 do VDR, BsmI (rs1544410 G>A) e ApaI (rs7975232 G>T), localizados no intrão 8, e TaqI (rs731236 T>C), localizado no exão 9 do VDR. Estes quatro polimorfismos foram analisados com o objetivo de verificar de que forma influenciam a predisposição de um indivíduo para o desenvolvimento de cancro da tiróide. Desta forma, este estudo realizado na população Portuguesa, fez a análise destas variantes do VDR, e o seu impacto no desenvolvimento de cancro da tiróide de acordo com os seguintes parâmetros: tipo de cancro, idade de diagnóstico, sexo, dimensões do carcinoma, metástases ganglionares e à distância, multicentricidade tumoral, e estádios de cancro. Todos os participantes deste estudo foram indivíduos caucasianos de origem Portuguesa. Estes indivíduos foram divididos em dois grupos distintos. Um dos grupos foi composto por indivíduos com cancro diferenciado da tiróide (N = 208), provenientes do Instituto Português de Oncologia de Coimbra. O grupo de indivíduos saudáveis (N = 248), que constituíam o grupo controlo, consistiram em dadores voluntários de sangue Portugueses caucasianos, que não possuíam um historial clínico de cancro da tiróide. Após o recrutamento dos indivíduos e obtenção das amostras de sangue dos mesmos, procedeu-se a uma série de metodologias práticas que visaram como objetivo final genotipar as amostras recolhidas. A cada indivíduo, doente ou controlo, foi atribuído um número de código único, de forma a poder identificar e diferenciar a amostra em estudo. O processo clínico dos doentes foi registado com todos os dados necessários para este estudo. Quanto aos indivíduos saudáveis, estes permaneceram no anonimato, sendo apenas registado a idade, sexo, peso, altura e naturalidade. Após estes procedimentos de registo, o DNA genómico foi extraído das amostras de sangue recolhidas através do método de “salting-out”. De seguida o DNA extraído foi quantificado e armazenado. Para efeitos de genotipagem, o DNA de cada indivíduo participante no estudo foi submetido à técnica “polymerase chain reaction”, mais conhecida por PCR. Com este procedimento pretende-se amplificar o fragmento do gene VDR onde se encontra cada polimorfismo. Após a amplificação do fragmento do VDR que se pretendeu estudar, conforme o polimorfismo, procedeu-se à digestão enzimática utilizando a respetiva enzima. Desta forma, conseguimos determinar o genótipo do indivíduo, através da visualização desses produtos digeridos num gel de agarose de 3%. Para além deste método, a genotipagem foi também confirmada através da sequenciação de DNA, sendo utilizada uma amostra representativa de cada genótipo para cada polimorfismo. Terminada a genotipagem de todos os indivíduos participantes deste estudo, para os quatro polimorfismos do VDR, procedeu-se ao tratamento estatístico dos dados analisando os parâmetros acima referidos. Como resultados, verificaram-se, em alguns parâmetros, algumas diferenças de frequências dos polimorfismos. De entre esses resultados, nas comparações entre pacientes de sexo diferente, o genótipo GA do polimorfismo BsmI foi mais frequente no sexo masculino (p = 0.044). Na análise de metástases ganglionares e à distância, o genótipo AA (p = 0.004) do BsmI e o alelo A (p = 0.014) e o genótipo CC (p = 0.024) do TaqI foram mais frequentes no grupo de doentes com metástases. No estudo da multicentricidade tumoral, o alelo C (p = 0.041) do FokI, o genótipo AA (p = 0.013) do BsmI, e o genótipo CC (p = 0.017) do TaqI foram mais frequentes nos doentes com multicentricidade. No estudo dos estádios de cancro, os genótipos GT (p = 0.012) e TT (p = 0.004) do ApaI, e seu respetivo alelo T (p = 0.031) foram mais frequentes em doentes com estádios mais avançados. A correção estatística de Bonferroni para comparações múltiplas revelou que os resultados foram estatisticamente significativos apenas para o genótipo AA do polimorfismo BsmI, que parece estar envolvido na presença de metástases ganglionares em indivíduos com cancro diferenciado da tiróide. Para além disso, também o genótipo TT do polimorfismo ApaI revelou diferenças estatisticamente significativas, podendo estar associado a um estádio mais avançado de cancro da tiróide. Desta forma, os polimorfismos do gene do VDR podem servir como marcadores de risco úteis para pacientes com cancro diferenciado da tiróide, uma vez que estes já forma associados em outros tipos de cancro. No entanto, não é possível retirar conclusões a partir destes resultados uma vez que são necessários mais estudos que permitam compreender as ações celulares e moleculares do VDR. Para tal, estudos funcionais genómicos serão necessários, para que se possa clarificar de que forma os polimorfismos deste gene podem influenciar a suscetibilidade genética para o cancro da tiróide.
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Schuch, Natielen Jacques. "Relação entre as concentrações séricas da vitamina D, polimorfismos do gene do VDR e síndrome metabólica em adultos e idosos." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/6/6138/tde-20012012-093621/.

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Introdução - O receptor de vitamina D (VDR) é expresso em vários tecidos e quando este se encontra na sua forma ativada, modula a expressão de diversos genes. Esses incluem variações dos níveis circulantes de 1,25(OH) 2 D , variações na densidade mineral óssea, secreção e sensibilidade à insulina em resposta à glicose, suscetibilidade à diabetes tipo 1 e 2, obesidade, dislipidemias e hipertensão arterial. Atualmente, evidências têm sugerido o envolvimento da vitamina D com a síndrome metabólica. Objetivo - Investigar a concentração sérica da vitamina D e sua relação com a síndrome metabólica e avaliar a potencial associação entre estes fatores com a presença de polimorfismos no gene do receptor de vitamina D (VDR) em indivíduos adultos. Métodos - Trata-se de um estudo transversal, onde foram avaliados 372 indivíduos adultos. Foram coletadas amostras sanguíneas para dosagens laboratoriais da 25(OH)D 3 , PTH e exames bioquímicos relacionados à SM, além disso foram realizadas avaliações antropométricas (peso, altura, IMC). A síndrome metabólica (SM) foi classificada usando o critério proposto pelo National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATP III). A resistência a insulina foi estimada pelo cálculo de HOMA IR e a função da célula pelo cálculo de HOMA . A 25(OH)D foi dosada por HPLC e a insuficiência foi determinada pelo ponto de corte da curva Roc (52,6nmol/l). Foram avaliados também PTH intacto e cálcio sérico. Os polimorfismos BsmI e FokI foram detectados através da digestão das enzimas de restrições específicas para cada polimorfismo e confirmados através da técnica PCR alelo específico (ASPCR) ou amplificação de mutação refratária (ARMs) nos indivíduos com e sem SM (52 por cento vs. 48 por cento , respectivamente). A análise estatística inclui construção da curva ROC, teste T de Student, testes de correlação, teste de equilíbrio de Hardy-Weinberg, ANOVA, regressão logística binária (Odds Ratio). Estas análises foram conduzidas no software SPSS para Windows, versão 18 e p < 0,05 foi considerado significante. Resultados - A idade média dos participantes foi 51(15) anos, o IMC médio 29(6) kg/m 3 2 e 48 por cento apresentaram SM. Como esperado, os 3 indivíduos com SM apresentaram maiores valores de idade 57(12) anos, IMC 32(6) Kg/m , circunferência de cintura 103(13) cm, pressão sistólica 138(17) mmHg e diastólica 83(10) mmHg, glicemia de jejum 98(12) mg/dl, triglicérides 165(76) mg/dl, índices HOMA-IR 2.2(1.7) e 116(95), e menores valores de colesterol HDL colesterol 41(11) mg/dl. Com relação às concentrações séricas de 25(OH)D propostas pela análise da curva ROC, 43 por cento dos indivíduos com SM e 57 por cento dos indivíduos sem SM apresentam insuficiência desta vitamina. Correlações entre 25(OH)D 3 3 com PTH (r = -0.153; p = 0.005) e com circunferência da cintura (r = -0.106; p = 0.05) foram observada em todos os participantes. Considerando os polimorfismos do gene VDR, nos pacientes com SM, não houve associação entre o polimorfismo BsmI e os componentes da SM, HOMA e IR, 25(OH)D e PTH. No entanto, indivíduos sem SM, mas com homozigose para polimorfismo BsmI (genótipo recessivo bb ), apresentaram concentrações mais baixas de 25(OH)D 3 3 do que aqueles com o genótipo BB normal. Além disso, os indivíduos com SM e heterozigose para o polimorfismo FokI (genótipo Ff) têm maiores concentrações de PTH e HOMA do que aqueles com genótipo normal FF. Nesse mesmo grupo, os indivíduos com o genótipo recessivo ff têm maior resistência à insulina do que aqueles com genótipo Ff. Por outro lado, os pacientes sem SM, mas carregando o genótipo Ff, apresentaram maiores concentrações de triglicerídeos e baixos níveis de HDL do que aqueles com genótipo FF. A presença de um alelo f no genótipo (Ff ou ff) é, aparentemente, o suficiente para aumentar os níveis de triglicérides e resistência à insulina, quando comparados ao genótipo normal FF. Conclusão - Os resultados demonstram que o polimorfismo FokI no gene VDR associa-se a resistência à insulina e maiores concentrações de PTH em pacientes que apresentam SM. Além disso, o polimorfismo BsmI associa-se a menores concentrações de 25(OH)D em indivíduos sem SM. Portanto, esses novos dados indicam que polimorfismos no gene do VDR estão associados a diferentes fenótipos dos componentes da SM
Introduction - The vitamin D receptor (VDR) is expressed in many tissues and when it is in its activated form modulates the expression of several genes. These include changes in circulating levels of 1,25(OH)2D3, variations in bone mineral density, sensitivity and secretion of insulin in response to glucose, susceptibility to type 1 and 2 diabetes mellitus, obesity, dyslipidemia and hypertension. Currently, evidences have suggested the involvement of vitamin D with the metabolic syndrome. Objective - To investigate the serum concentrations of vitamin D and its relationship with metabolic syndrome (MS) and to evaluate the potential association between these factors with the presence of polymorphisms in vitamin D receptor gene in individuals adults. Methods - This is a cross-sectional study, which evaluated 243 adults and elderly. We collected blood samples for measurements of 25(OH)D3, iPTH, biochemical tests related to MS, and anthropometric evaluation (weight, height, BMI) were also assessed. MS was classified using the criteria proposed by the National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATP III). Insulin resistance and cell secretion were estimated by calculating HOMA IR and HOMA , respectively. The 25(OH)D3 was measured by HPLC and insufficiency was determined by the Roc curve cut-off (52.6 nmol/L). Intact PTH and serum calcium were also evaluated. The BsmI and FokI polymorphisms were detected by enzymatic digestion with specific enzymes and confirmed by allele specific PCR (ASPCR) or amplification of refractory mutation (ARM) in individuals with or without MS (52 per cent vs. 48 per cent , respectively). Statistical analyses include construction of Roc curves, Student T test, correlation tests, Hardy-Weinberg test, ANOVA, binary logistic regression (odds ratio), and TwoStep Cluster. These analyses were conducted with SPSS for Windows, version 18 and p < 0.05 was considered significant. Results - The mean age of participants was 51(15) years, mean BMI was 29(6) kg/m2, and 48 per cent of individuals presented MS. As expected, subjects with MS showed higher values of age (57(12) years), BMI was 32(6) kg/m2, waist circumference was 103(13) cm, systolic blood pressure was 138(17) mmHg, diastolic was 83(10) mmHg, fasting glucose was 98(12) mg/dl, triglycerides was 165(76) mg/dl, HOMA-IR was 2.2(1.7), HOMA was 116(95), and lower levels of HDL cholesterol was observed (41 mg/dl(11)). With respect to serum 25(OH)D3 proposed by ROC curve analysis, 43 per cent of individuals with MS and 57 per cent of individuals without MS presented insufficiency of this vitamin. Correlations between 25(OH)D3, iPTH (r = -0,153, p = 0.005), and waist circumference (r = -0,106, p = 0.05) were observed in all participants. Considering the VDR gene polymorphisms, in patients with MetSyn, there is no association among BsmI polymorphism and components of MetSyn, HOMA IR and , 25(OH)D3, and PTH. However, subjects without MetSyn, but with homozygosis for BsmI polymorphism (recessive bb genotype), presented lower levels of 25(OH)D3 than those with normal BB genotype. In addition, individuals with MetSyn and heterozygosis for FokI polymorphism (Ff genotype) have higher concentrations of PTH and HOMA than those with normal FF genotype. In this same group, subjects with the recessive ff genotype have higher insulin resistance than those with Ff genotype. On the other hand, patients without MetSyn, but carrying the Ff genotype, have higher concentration of triglycerides and lower levels of HDL than those with FF genotype. Interestingly, the presence of one allele f in the (Ff or ff) genotype is apparently enough to increase triglycerides levels and insulin resistance, when compared to the normal FF genotype. Conclusion - The results show that FokI polymorphism in the VDR gene is associated to insulin resistance and higher concentrations of PTH in patients with MetSyn. Moreover, BsmI polymorphism is related to a lower concentration of 25(OH)D3 in individuals without MetSyn. Therefore, the results indicated that VDR gene polymorphisms are associated to different phenotypes of MetSyn components
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Kommagani, Ramakrishna. "DIFFERENTIAL REGULATION OF VITAMIN D RECEPTOR (VDR) BY p53, p63 AND p73." Wright State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=wright1239687284.

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Caus, Enríquez Maite. "La ausencia de VDR en CMLV previene la calcificación vascular en ERC: Potencial rol del miR-145a." Doctoral thesis, Universitat de Lleida, 2021. http://hdl.handle.net/10803/671528.

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La calcificació vascular (CV) es una complicació molt prevalent en la malaltia renal crònica (MRC) i s’associa amb una alta mobilitat i mortalitat en pacients amb MRC. El receptor de la vitamina D (VDR) s’ha considerat que té un rol important en la diferenciació osteoblástica de les cèl·lules de múscul llis vascular (CMLV), tot i que el mecanisme concret encara no està clar. A més a més, la capacitat de VDR per influir en l’expressió de varis microRNAs (miRNAs), així com la gran quantitat de miRNAs presents en les CMLV, ens fa enfocar-nos en aquestes petites molècules com importants reguladores de la diferenciació i modulació fenotípica de les CMLV. L’objectiu d’aquest estudi va ser avaluar l’efecte de la deficiència de VDR en la calcificació vascular en MRC i la possible implicació del miR-145a en aquest procés. Vam confirmar un increment de tinció immunohistoquímica de VDR juntament amb un nivells augmentats de calci en arteries epigàstriques de pacients amb MRC comparat amb arteries de donants sans. Els ratolins amb nefrectomia 5/6 també mostraven alts nivells de calci arterial i de tinció immunohistoquímica de VDR comparat amb els ratolins controls. Els ratolins knockout condicionals per VDR en CMLV (Cre+ VDRlox/lox) sotmesos a una nefrectomia i tractats amb dieta alta en fòsfor i calcitriol van mostrar nivells significativament més baixos de contingut de calci, expressió d’osteopontina i lamin A, així com uns nivells més alts d’expressió de SOST comparat amb ratolins Cre+ VDRwt/wt amb el mateix tractament. A més a més, els ratolins Cre+ VDRwt/wt amb ERC i CV mostraven significativament nivells més baixos d’expressió arterial del miR-145a comparat amb els ratolins amb una eliminació específica de VDR en CMLV. In vitro, les CMLV VDRwt tractades amb medis calcificants mostraven nivells més alts de calci que les CMLV VDRko, juntament amb un increment de OPN a nivell de mRNA i proteïna. Els nivells del miR-145a disminuïen en CMLV amb condicions calcificants, tant en VDRwt com en VDRko, contràriament als resultats in vivo. Mitjançant la transfecció del miR-145a vam detectar un lleuger descens de la calcificació i de l’expressió de OPN en condicions calcificants. Concloem que l’eliminació del VDR de les CMLV protegeix enfront la calcificació vascular en MRC i que els mecanismes que regulen aquesta CV poden involucrar al miR-145a.
La calcificación vascular (CV) es una complicación muy prevalente en la enfermedad renal crónica (ERC) y se asocia con la alta morbilidad y mortalidad en estos pacientes. El receptor de la vitamina D (VDR) se ha considerado que tiene un rol importante en la diferenciación osteoblástica de las células de musculo liso vascular (CMLV), aunque el mecanismo preciso aún no es claro. La capacidad de VDR para influenciar la expresión de varios microRNAs (miRNAs), así como la gran cantidad de miRNAs presentes en CMLV, nos hizo prestar atención a estas pequeñas moléculas como posibles reguladoras del cambio fenotípico de las CMLV. El objetivo de este estudio fue evaluar el efecto de la deficiencia de VDR en la calcificación vascular en ERC y la posible implicación del miR-145a en este proceso. Confirmamos un incremento de tinción inmunohistoquímica de VDR juntamente con unos niveles más altos de calcio en arterias epigástricas de pacientes con ERC comparado con arterias de donantes sanos. Así como también, ratones con nefrectomía 5/6 mostraban altos niveles de calcio arterial y tinción inmunohistoquímica de VDR comparado con los ratones controles. Los ratones knockout condicionales para VDR en CMLV (Cre+ VDRlox/lox) sujetos a una nefrectomía y tratados con dieta alta en fosforo y calcitriol, mostraron niveles significativamente disminuidos de contenido de calcio, de expresión de osteopontina y lamin A, así como unos niveles más altos de expresión de SOST en arteria comparado con los ratones Cre+ VDRwt/wt con el mismo tratamiento. Además, los ratones Cre+ VDRwt/wt con ERC y CV, mostraron una disminución significativa del miR-145a comparado con los ratones con Cre+ VDRlox/lox. In vitro, las CMLV VDRwt con medios calcificantes mostraron niveles más altos de calcio que las CMLV VDRko, junto con un incremento de OPN. Los niveles del miR-145a disminuían en CMLV con condiciones calcificantes, tanto en VDRwt como en VDRko, contrariamente a los resultados in vivo. Mediante la transfección del miR-145a detectamos un ligero descenso del calcio y la expresión de OPN en condiciones calcificantes. Concluimos que la eliminación de VDR de las CMLV previene la calcificación vascular en ERC y que los mecanismos que regulan esta CV pueden involucrar al miR-145a.
Vascular calcification (VC) is a highly prevalent complication of chronic kidney disease (CKD) and, when present, is associated with the higher morbidity and mortality in CKD patients. Vitamin D receptor (VDR) has been proposed to have an important role in the osteoblastic differentiation of vascular smooth muscle cells (VSMCs); nevertheless the precise mechanism is unclear. The potential of VDR to influence widespread microRNAs (miRNAs) expression, as well as a myriad of miRNAs present in VSMCs drew attention to these small molecules as important regulators of VSMCs differentiation and phenotypic modulation. The aim of this study was to evaluate the effect of VDR deficiency on vascular calcification in CKD and the possible involvement of miR-145a in this process. We confirmed an increase of VDR immunostaining together with higher calcium in epigastric arteries from CKD patients compared with arteries from control non-CKD donors. We next analysed arteries from mice subjected to 5/6 nephrectomy. CKD affected mice showed higher levels of calcium content and VDR immunostaining in their arteries compared with control mice. VSMC-VDR conditional knockout mice (Cre+ VDRlox/lox) subjected to a subtotal nephrectomy and treated with high phosphate diet plus calcitriol showed significantly lower levels of vascular calcium content, osteopontin and lamin A expression, as well as markedly higher levels of SOST expression compared with their counterparts (Cre+VDRwt/wt) on the same treatment. Cre+VDRwt/wt mice affected by CKD and presenting VC showed significantly lower levels of expression of arterial miR-145a compared with mice with targeted deletion of VDR in VSMCs. In vitro, VDRwt VSMCs treated with calcification medium demonstrated higher levels of calcification than VDRko VSMCs, alongside an increased OPN. Levels of miR-145a decreased in VSMC with calcification conditions, both in VDRwt, which developed calcification, and in VDRko in which we didn’t detect calcium previously, contrarily to in vivo results. Through miR-145a transfection we detect a slight decrease in calcium and OPN expression in calcification conditions We conclude that VSMC’s VDR elimination prevents vascular calcification in CKD and that the mechanisms regulating VC might involve miR-145a, which warrant further investigations in this direction.
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Han, Shuxin. "VITAMIN D RECEPTOR REGULATION OF CHOLESTEROL 7α-HYDROXYLASE GENE TRANSCRIPTION AND BILE ACID SYNTHESIS IN HUMAN HEPATOCYTES." Kent State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=kent1257459841.

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Jain, Reema. "When too much sun is never enough: Association of the VDR gene polymorphisms with insulin resistance." AUT University, 2010. http://hdl.handle.net/10292/990.

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The metabolism of vitamin D commences with exposure of the skin to sunlight. The growing recognition of its role in insulin resistance, autoimmune disorders, infections, cancer, as well as the health of cells that influence physical and mental function have profound implications on how we define vitamin D requirements and why we should care whether they are met or not. Most of the actions of vitamin D are mediated by the vitamin D receptor (VDR), a protein whose gene sequence can vary, giving rise to polymorphic forms which are potent enough to affect the binding capacity of this protein to vitamin D. Some of these polymorphic forms of VDR gene may be associated with reduced effectiveness of vitamin D and hence predispose individuals to diseases such as type 2 diabetes and insulin resistance. An earlier study, the Surya Study, looked at the responsiveness of the South-Asian women living in Auckland to vitamin D. The research described here is an extension of this study and its focus was to identify the associations/linkages between certain polymorphic forms of the VDR gene and the disease conditions and intervention responsiveness in the same women. The first objective was to compare two well known techniques for genotyping single nucleotide polymorphisms (SNPs) of the VDR gene at the 3’ end, namely BsmI, ApaI and TaqI: the newer real-time polymerase chain reaction (qPCR) and the traditional restriction fragment length polymorphism polymerase chain reaction (RFLP-PCR) techniques. This comparison was performed to evaluate alternative methods for genotyping which consumed less time than RFLP-PCR. When the presence of each polymorphism by both the techniques was compared in this cohort of South-Asian women, it was found that RFLP-PCR proved to be a more reliable technique than qPCR for genotyping the VDR gene. Another objective of this project was to investigate the prevalence of the above three polymorphisms along with Cdx-2 and FokI SNPs which are present at the 5’ end of the VDR gene, in the population under study and their possible association with phenotypes such as vitamin D responsiveness and insulin resistance. These women were screened and biochemical data was collected during the earlier Surya Study. Of these, eighty-one women were then selected for intervention based on them having high insulin resistance (HOMA-IR>1.93) and serum 25(OH)D<50 nmol/L. Out of these eighty-one women, forty-two were given vitamin D supplement and thirty-nine were given a placebo for six months. Baseline and endpoint measurements included insulin resistance (HOMA-IR), insulin sensitivity (HOMA2%S) etc. How each individual responded to treatment in the intervention group was analysed in the context of the polymorphisms that they had. An association of insulin resistance with BsmI, ApaI and TaqI SNPs was observed in this cohort of 239 women. The response to insulin resistance in the vitamin D supplemented group significantly differed for FokI genotype compared to other genotypes. This explained why certain women responded to treatment better than the others. When the frequencies of the genotypes of these five SNPs of the VDR gene were compared to other studies of different ethnicities, the results of this study were consistent with few studies but contradictory to others. The possible reasons for these differences could be because of small sample size and different ethnicities under study due to which the frequency of alleles and hence the genotypes differed.
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Zhang, Xi [Verfasser], and Nadia [Akademischer Betreuer] Harbeck. "Potential new biomarkers for breast cancer : Vitamin D receptor (VDR) and BRCA1 proteins / Xi Zhang ; Betreuer: Nadia Harbeck." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1159879672/34.

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Joshi, Amod N. "Analysis of Archived Dried Blood Spots by Mass Spectrometry for Vitamin D and Real-time PCR for its Enzymes and Receptor." Wright State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=wright1323273377.

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Chen, Jiaxuan. "The role of Pdia3 in vitamin D signaling in osteoblasts." Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/50147.

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1a,25-Dihydroxyvitamin D3 (1a,25(OH)2D3) is a major functional metabolic form of vitamin D. 1a,25(OH)2D3 has drawn increasing attention due to its functions in addition to maintaining calcium phosphate homeostasis. It directly regulates mineralization by osteoblasts, matrix production and remodeling by chondrocytes, and contraction of cardiomyocytes. 1a,25(OH)2D3 and its analogues have shown beneficial effects in treating multiple sclerosis, diabetes and various types of cancer. In order to maximize the pharmaceutical potential of 1a,25(OH)2D3, a better understanding its cell signaling pathway is necessary. 1a,25(OH)2D3 regulates osteoblasts through both classical nuclear vitamin D receptor (nVDR) mediated genomic effects and plasma membrane receptor-mediated rapid responses. The identity of the plasma membrane receptor for 1a,25(OH)2D3 is controversial. Protein disulfide isomerase associated 3 (Pdia3) has been hypothesized as one of the putative plasma membrane receptors for 1a,25(OH)2D3. The overall goal of this thesis was to understand the general role and the molecular mechanism of Pdia3 in 1a,25(OH)2D3-initiated rapid responses, and to determine the role of Pdia3 and its dependent signaling in osteoblast biology. The results show that Pdia3 is required for membrane-mediated responses of 1a,25(OH)2D3. Moreover, both Pdia3 and nVDR are critical components of the plasma membrane receptor complex for 1a,25(OH)2D3. Finally, Pdia3 and signaling via Pdia3 regulate osteoblast differentiation and mineralization. Taken together, this study demonstrates the role of Pdia3 in rapid responses to 1a,25(OH)2D3 and osteoblast biology, reveals the unexpected complexity of the 1a,25(OH)2D3 plasma receptor complex and opens the new target, Pdia3, for pharmaceutical application and tissue engineering.
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Books on the topic "Vitamin D Receptor (VDR)"

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Eleftheriadis, Theodoros. Vitamin D receptor agonists and kidney diseases. Hauppauge, N.Y: Nova Science Publishers, 2010.

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Gardner, Philip P. Human vitamin D receptor polymorphisms: A molecular and population analysis. [s.l.]: typescript, 1998.

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Trang, Hoang. The effects of vitamin D and its receptor in normal subjects and kidney stone formers. Ottawa: National Library of Canada, 1998.

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Egwuekwe, Ejike R. Vitamin d Receptor Gene Polymorphisms and the Risks of Breast Cancer. iUniverse, Incorporated, 2020.

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Vitamin D3 Analogues with Low Vitamin D Receptor Binding Affinity Regulate Chondrocyte Proliferation, Proteoglycan Synthesis, and Protein Kinase C Activity. Storming Media, 1997.

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Segaert, Siegfried. The Role of 1a,25-Dihydroxyvitamin D3 and the Vitamin D Receptor in the Control of Proliferation and Differentiation of the Epidermal Keratinocyte (Acta Biomedica Lovaniensia 196). Leuven Univ Pr, 1999.

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Jadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0146_update_001.

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Disorders of bone mineralization cause rickets in children and osteomalacia in adults. Both remain common in developing countries. Incidence in Western countries had declined since the fortification of foodstuffs, but appears to be increasing again. Calcium and inorganic phosphate are the key precursors for bone mineralization and growth. The commonest aetiology of osteomalacia is vitamin D deficiency, primarily due to low dietary intake and inadequate sun exposure. In the last decade gene mutations have been identified that are responsible for inherited rickets and osteomalacia, particularly those that result in phosphate deficiency, hypophosphatasia, and vitamin D receptor or metabolizing enzyme mutations. Additionally, the pathogenesis of tumour-induced osteomalacia is becoming better understood. Osteomalacia may present as bone pain and tenderness, muscle pain and weakness, and skeletal deformity or fracture. Key investigations include biochemical assessment and plain radiographs. Radioisotope bone scans and bone biopsy may be considered in selected cases. Differential diagnoses include osteoporosis, seronegative arthritides, and localized soft tissue disorders. Treatment, guided by the underlying aetiology, aims to reduce symptoms, fracture risk, bone deformity and sequelae. Vitamin D deficient patients require vitamin D and calcium replacement.
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Jadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0146.

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Disorders of bone mineralization cause rickets in children and osteomalacia in adults. Both remain common in developing countries. Incidence in Western countries had declined since the fortification of foodstuffs, but appears to be increasing again. Calcium and inorganic phosphate are the key precursors for bone mineralization and growth. The commonest aetiology of osteomalacia is vitamin D deficiency, primarily due to low dietary intake and inadequate sun exposure. In the last decade gene mutations have been identified that are responsible for inherited rickets and osteomalacia, particularly those that result in phosphate deficiency, hypophosphatasia, and vitamin D receptor or metabolizing enzyme mutations. Additionally, the pathogenesis of tumour-induced osteomalacia is becoming better understood. Osteomalacia may present as bone pain and tenderness, muscle pain and weakness, and skeletal deformity or fracture. Key investigations include biochemical assessment and plain radiographs. Radioisotope bone scans and bone biopsy may be considered in selected cases. Differential diagnoses include osteoporosis, seronegative arthritides, and localized soft tissue disorders. Treatment, guided by the underlying aetiology, aims to reduce symptoms, fracture risk, bone deformity and sequelae. Vitamin D deficient patients require vitamin D and calcium replacement.
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Trepiccione, Francesco, and Giovambattista Capasso. Calcium homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0026.

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Ca2+ homeostasis is achieved through a fine balance among three main organs: the intestine, the kidney, and bone. Blood levels of Ca2+ are accurately tuned through the Ca2+ sensing receptors and regulated by several hormones, including parathyroid hormone (PTH), active vitamin D, and calcitonin. The most recent findings in Ca2+ handling are described. The role of the Ca2+ sensing receptor, as well as Klotho, a new player participating in Ca2+ homeostasis, are described. Finally, the effects of diuretics, calcineurin inhibitors, and the link between hypertension and Ca2+ metabolism are reviewed.
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Gutiérrez, Orlando M. Fibroblast growth factor 23, Klotho, and phosphorus metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0119.

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Fibroblast growth factor 23 (FGF23) and Klotho have emerged as major hormonal regulators of phosphorus (P) and vitamin D metabolism. FGF23 is secreted by bone cells and acts in the kidneys to increase urinary P excretion and inhibit the synthesis of 1,25 dihydroxyvitamin D (1,25(OH)2D) and in the parathyroid glands to inhibit the synthesis and secretion of parathyroid hormone. Phosphorus excess stimulates FGF23 secretion, likely as an appropriate physiological adaptation to maintain normal P homeostasis by enhancing urinary P excretion and diminishing intestinal P absorption via lower 1,25(OH)2D. The FGF23 concentrations are elevated early in the course of chronic kidney disease (CKD) and may be a primary initiating factor for the development of secondary hyperparathyroidism in this setting. Klotho exists in two forms: a transmembrane form and a secreted form, each with distinct functions. The transmembrane form acts as the key co-factor needed for FGF23 to bind to and activate its cognate receptor in the kidneys and the parathyroid glands. The secreted form of Klotho has FGF23-independent effects on renal P and calcium handling, insulin sensitivity, and endothelial function. Disturbances in the expression of Klotho may play a role in the development of altered bone and mineral metabolism in early CKD. In addition, abnormal circulating concentrations of both FGF23 and Klotho have been linked to excess cardiovascular disease, suggesting that both play an important role in maintaining cardiovascular health.
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Book chapters on the topic "Vitamin D Receptor (VDR)"

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Vázquez-Cedeira, Marta, Diana M. Monsalve, Marta Sanz-García, Pedro A. Lazo, Thierry Galli, Véronique Proux-Gillardeaux, Xosé R. Bustelo, et al. "Vitamin D receptor (VDR)." In Encyclopedia of Signaling Molecules, 1984. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101456.

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Vázquez-Cedeira, Marta, Diana M. Monsalve, Marta Sanz-García, Pedro A. Lazo, Thierry Galli, Véronique Proux-Gillardeaux, Xosé R. Bustelo, et al. "VDR, The Vitamin D Receptor." In Encyclopedia of Signaling Molecules, 1977–84. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_287.

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von Essen, Marina Rode, and Carsten Geisler. "VDR, the Vitamin D Receptor." In Encyclopedia of Signaling Molecules, 5907–14. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_287.

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von Essen, Marina Rode, and Carsten Geisler. "VDR, the Vitamin D Receptor." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_287-1.

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Capiati, Daniela, Graciela Santillán, Ana Rossi, Paula Monje, and Ricardo Boland. "Nuclear Vitamin D (VDR) and Estrogen (ER) Receptors in the Membrane of Muscle and Breast Cancer Cells." In The Identities of Membrane Steroid Receptors, 57–65. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0339-2_7.

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Barsony, Julia. "VDR and RXR Subcellular Trafficking." In Vitamin D, 153–73. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-303-9_6.

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Thorne, James, and Moray J. Campbell. "The Molecular Cancer Biology of the VDR." In Vitamin D and Cancer, 25–52. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7188-3_2.

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Yamada, S., M. Shimizu, and K. Yamamoto. "Vitamin D Receptor." In Vitamin D and Rickets, 50–68. Basel: KARGER, 2003. http://dx.doi.org/10.1159/000072769.

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Dowd, Diane R., and Paul N. MacDonald. "The Molecular Biology of the Vitamin D Receptor." In Vitamin D, 135–52. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-303-9_5.

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Bikle, Daniel D. "The Vitamin D Receptor." In Sunlight, Vitamin D and Skin Cancer, 282–302. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0437-2_16.

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Conference papers on the topic "Vitamin D Receptor (VDR)"

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Guzeeva, Olga, Irina Melnikova, Valentina Larionova, Valeria Novikova, and Diana Kuzmina. "GP142 Level of 25(OH)-vitamin D and vitamin D receptor (VDR) gene polymorphisms in adolescents with chronic gastroduodenitis." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.206.

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Horas, K., M. Abraham, F. Jakob, R. Ebert, G. Maier, BM Holzapfel, and M. Rudert. "Deprivation of the vitamin D receptor (VDR) fuels breast cancer metastases to bone." In OSTEOLOGIE 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1679962.

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Cabang, April B., Jay L. Morris, and Michael J. Wargovich. "Abstract A03: Determining the role of Vitamin D Receptor (VDR) and Retinoid X Receptor Alpha (RXRα) in colitis." In Abstracts: AACR Special Conference: Colorectal Cancer: From Initiation to Outcomes; September 17-20, 2016; Tampa, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.crc16-a03.

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Gantes, M., A. Arteaga, Y. Barrios, I. Ferraz, A. Alvarez, B. Rodríguez-Lozano, D. Batista, E. Trujillo, and T. González. "AB0186 Changes in bone turnover markers and vitamin d receptor (vdr) genotype during glucocorticoid therapy." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.625.

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Gantes, M., A. Arteaga, Y. Barrios, E. Uruburu, I. Ferraz, B. Rodríguez-Lozano, A. Alvarez, E. Trujillo, and T. González. "SAT0169 Influence of vitamin d receptor (vdr) genotype in the bone loss induced by corticosteroid therapy." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.656.

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Tavera, Luz E., Thomas Westerling, and Myles Brown. "Abstract LB-275: Genome-wide analysis of the vitamin D receptor (VDR) binding sites reveals vitamin D role mediating autophagy in luminal-like breast cancer cells." 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-lb-275.

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Poulin, Matthew L., Ann Meyer, Gregory Gonzalez, Kevin Bi, and Liying Yan. "Abstract 4242: Methylation, SNP and expression analysis of the Vitamin D receptor (VDR) gene in different tumor tissues." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4242.

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Tavera, Luz E., Thomas Westerling, and Myles Brown. "Abstract 3562: Genome-wide analysis of the vitamin D receptor (VDR) binding sites reveals vitamin D role modulating autophagy and metabolism in luminal-like breast cancer cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3562.

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Yousif, Sara O., Amar M. Ismail, Abdelrahim O. Mohamed, and Abdelrahim O. Mohamed. "Abstract 1455: Vitamin D receptor (VDR) gene polymorphisms among Sudanese females with breast cancer attending Radio and Isotope Center of Khartoum." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1455.

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Poon, Audrey, Michael H. Cho, David Sparrow, and Augusto A. Litonjua. "A Variant In The Vitamin D Receptor Gene (VDR) Is Associated With Time To Onset Of Chronic Obstructive Pulmonary Disease (COPD) In Men." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2655.

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Reports on the topic "Vitamin D Receptor (VDR)"

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Narvaez, Carmen J., and JoEllen Welsh. The Role of VDR Phosphorylation in Vitamin D-Induced Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada392479.

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Baron, John A. Androgen and Vitamin D Receptor Gene Polymorphisms and Breast Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, October 2000. http://dx.doi.org/10.21236/ada393917.

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Bikle, Daniel D. The Tumor Suppressor Actions of the Vitamin D Receptor in Skin. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada614241.

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Baron, John A. Androgen and Vitamin D Receptor Gene Polymorphisms and Breast Cancer Risk. Fort Belvoir, VA: Defense Technical Information Center, October 2002. http://dx.doi.org/10.21236/ada413636.

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Bikle, Daniel D. The Tumor Suppressor Actions of the Vitamin D Receptor in Skin. Fort Belvoir, VA: Defense Technical Information Center, August 2013. http://dx.doi.org/10.21236/ada605251.

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