Relevant bibliographies by topics / Functional Characterization

Academic literature on the topic 'Functional Characterization'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Functional Characterization"

1

Koles, Kate, Kenneth D. Irvine, and Vladislav M. Panin. "Functional Characterization ofDrosophilaSialyltransferase." Journal of Biological Chemistry 279, no. 6 (November 11, 2003): 4346–57. http://dx.doi.org/10.1074/jbc.m309912200.

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Fortenberry, Yolanda, Jae-Ryoung Hwang, Ekaterina V. Apletalina, and Iris Lindberg. "Functional Characterization of ProSAAS." Journal of Biological Chemistry 277, no. 7 (November 21, 2001): 5175–86. http://dx.doi.org/10.1074/jbc.m104531200.

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Eckford, Paul D. W., and Frances J. Sharom. "Functional Characterization ofEscherichia coliMsbA." Journal of Biological Chemistry 283, no. 19 (March 15, 2008): 12840–50. http://dx.doi.org/10.1074/jbc.m708274200.

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4

Brand, Martin D., and Hoi Shan Wong. "Functional Characterization of S1QELs." Free Radical Biology and Medicine 100 (November 2016): S31—S32. http://dx.doi.org/10.1016/j.freeradbiomed.2016.10.080.

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5

Varatharaju, G., K. Nithya, P. Suresh, M. Rekha, N. Balasubramanian, S. Gomathinayagam, P. T. Manoharan, and V. Shanmugaiah. "Biocontrol Properties and Functional Characterization of Rice Rhizobacterium Pseudomonas sp. VSMKU4036." Journal of Pure and Applied Microbiology 14, no. 2 (June 29, 2020): 1545–56. http://dx.doi.org/10.22207/jpam.14.2.53.

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6

Simpson, Jeremy C., and Arwyn T. Jones. "Early endocytic Rabs: functional prediction to functional characterization." Biochemical Society Symposia 72 (January 1, 2005): 99–108. http://dx.doi.org/10.1042/bss0720099.

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Endocytic pathways are highly dynamic gateways for molecules to enter cells. Functionality and specificity is in part controlled by a number of small GTPases called Rabs. In defined cellular locations, Rabs mediate multiple functions in membrane trafficking via their specific interaction with organelle membranes and a host of affector and effector molecules. On endocytic pathways, Rabs have been shown to control the formation of vesicles on the plasma membrane and the downstream delivery of internalized molecules to a number of cellular locations. As numerous Rabs are located to endocytic pathways, an internalized molecule may traverse a number of Rab specific substations or subdomains en route to its final destination. Rabs 5, 21 and 22 have all been localized to the early endocytic pathway and have been shown to share a number of characteristics to merit their segregation into a single functional endocytic group. In this review, we compare experiments that describe similarities and differences in endosome morphology and function that is mediated by their expression in cells.
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Dhingani, Rashmin M., Manoj V. Parakhia, Rukam S. Tomar, Bipin J. Malviya, and B. A. Golakiya B. A. Golakiya. "Functional characterization of PGPR and its identification through 16 S rRNA sequencing." Indian Journal of Applied Research 3, no. 6 (October 1, 2011): 47–50. http://dx.doi.org/10.15373/2249555x/june2013/17.

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8

Amato, R., and G. Marot. "Functional Characterization of Hydroxy-Polybutadienes." Journal of Liquid Chromatography 14, no. 1 (January 1991): 79–95. http://dx.doi.org/10.1080/01483919108049599.

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9

Corman, Etienne, and Maks Ovsjanikov. "Functional Characterization of Deformation Fields." ACM Transactions on Graphics 38, no. 1 (February 20, 2019): 1–19. http://dx.doi.org/10.1145/3292480.

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10

Schlicht, K. E., N. Michno, B. D. Smith, E. E. Scott, and S. E. Murphy. "Functional characterization of CYP2A13 polymorphisms." Xenobiotica 37, no. 12 (December 2007): 1439–49. http://dx.doi.org/10.1080/00498250701666265.

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Dissertations / Theses on the topic "Functional Characterization"

1

Sha, Sha, and 沙莎. "Functional characterization of cytoglobin." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46288739.

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Rossi, Fabio. "Functional characterization of WRNIP1." Thesis, Open University, 2012. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.580686.

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In order to guarantee cell survival, and the transmission of the correct genetic information to their offspring, organisms had to develop molecular pathways to deal with damaged genetic material and mechanisms to fix the damage. During their life, organisms are exposed to enormous amounts of DNA damage due both to mutagenic agents and normal environmental conditions. For instance, hydrolysis causes the release of up to 10000 purine bases from the DNA of a single cell per day. Therefore, DNA Damage Response (DDR) pathways comprise a variety of mechanisms including control and arrest of cell growth, tolerance of datpaged DNA, and DNA repair pathways. In this thesis, I focused on Wemer helicase interacting protein 1 (WRNIPl), and its role in the regulation of DDR. WRNIPl contains a single UBZ domain, which is also found in a group of proteins that are involved in DNA damage tolerance. Moreover WRNIP 1 is post-translationally modified with polyubiquitin chains and polyubiquitinylation is selectively induced after exposure to UV irradiation, suggesting that WRNIPl may have a role in the DNA damage response. Despite this evidence, the specific function of WRNIP 1 in mammalian cells remains unclear. To address this point, I have used different cell based viability assays and I have verified that the level of expression of WRNIP 1 negatively correlates with cell survival upon DNA damage. Significantly, down-regulation of WRNIPl results in a faster release from cell cycle check points, which is one of the main cellular responses to DNA damage. I have also found that these phenotypes are correlated with a WRNIP1-dependent negative regulation of DNA repair. Importantly, I have demonstrated that the effect of WRNIPl on these processes is dependent on the activity of the AAA + ATPase domain. Furthermore, my results on WRNIPl ubiquitinylation revealed that lysine 274 is specifically ubiquitinylated upon UV irradiation. Importantly, lysine 274 is a key residue for the Activity of the AAA+ ATPase, indicating that the ATPase activity of WRNIPl is impaired as part of the cellular response to UV damage. Taken together, these results suggest that WRNIPl functions as negative regulator of DNA repair, and that this function is specifically inhibited through ubiquitinylation when cells face UV-induced DNA damage.
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3

Bagchi, Rammyani. "Functional Characterization of Mtnip/latd’s Biochemical and Biological Function." Thesis, University of North Texas, 2013. https://digital.library.unt.edu/ark:/67531/metadc407822/.

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Symbiotic nitrogen fixation occurs in plants harboring nitrogen-fixing bacteria within the plant tissue. The most widely studied association is between the legumes and rhizobia. In this relationship the plant (legumes) provides the bacteria (rhizobia) with reduced carbon derived from photosynthesis in exchange for reduced atmospheric nitrogen. This allows the plant to survive in soil, which is low in available of nitrogen. Rhizobia infect and enter plant root and reside in organs known as nodules. In the nodules the bacteria fix atmospheric nitrogen. The association between the legume, Medicago truncatula and the bacteria Sinorhizobium meliloti, has been studied in detail. Medicago mutants that have defects in nodulation help us understand the process of nitrogen fixation better. One such mutant is the Mtnip-1. Mtnip-1 plants respond to S. meliloti by producing abnormal nodules in which numerous aberrant infection threads are produced, with very rare rhizobial release into host plant cells. The mutant plant Mtnip-1 has an abnormal defense-like response in root nodules as well as defects in lateral root development. Three alleles of the Mtnip/latd mutants, Mtnip-1, Mtlatd and Mtnip-3 show different degrees of severity in their phenotype. Phylogenetic analysis showed that MtNIP/LATD encodes a protein belonging to the NRT1(PTR) family of nitrate, peptide, dicarboxylate and phytohprmone transporters. Experiments with Mtnip/latd mutants demonstrats a defective nitrate response associated with low (250 μM) external nitrate concentration rather than high (5 mM) nitrate concentration. This suggests that the mutants have defective nitrate transport. To test if MtNIP/LATD was a nitrate transporter, Xenopus laevis oocytes and Arabidopsis thaliana mutant plants Atchl1-5, defective in a major nitrate transporter AtNRT1.1(CHL1), were used as surrogate expression systems. Heterologous expression of MtNIP/LATD in X. laevis oocytes and Atchl1-5 mutant plants conferred on them the ability to take up nitrate from external media with high affinity, thus demonstrating that MtNIP/LATD was a high affinity nitrate transporter. Km for MtNIP/LATD was determined to be approximately160 μM in the X. laevis system and 113 μM in the Arabidopsis Atchl1-5 mutant lines thus supporting the previous observation of MtNIP/LATD being a high affinity nitrate transporter. X. laevis expressing the mutant Mtnip-1 and Mtlatd, were unable to transport nitrate. However X. laevis oocytes, expressing the less severe mutant allele Mtnip-3 were able to transport nitrate suggesting another role of the Mtnip/latd besides high affinity nitrate transport. Experimental evidence suggested that MtNIP/LATD might transport another substrate beside nitrate. MtNIP/LATD levels are regulated by phytohormones. Experiments performed with ABA (abscisic acid), IAA (indole acetic acid) and histidine as substrates in X. laevis system show that the MtNIP/LATD mRNA injected oocytes efflux IAA but do not transport histidine or ABA. When wild type A17 and mutant Mtnip-1 and Mtnip-3 plants, grown in the presence of different sources of nitrogen were screened in herbicide chlorate, a structural analog of nitrate, the A17 and Mtnip-3 mutant showed levels of susceptibility that was different from mutant Mtnip-1 lines. Evidence suggested that the amount of chlorate transported into the plants were regulated by the C:N status of the A17 and Mtnip-3 plants. This regulation was missing in the Mtnip-1 lines thus suggesting a sensor function of MtNIP/LATD gene.
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4

Bojja, Aruna Sri. "Functional characterization of placental cathepsins." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 81 p, 2009. http://proquest.umi.com/pqdweb?did=1885754561&sid=4&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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5

Deshpande, Gopikrishna. "Nonlinear and network characterization of brain function using functional MRI." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/24760.

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Thesis (Ph.D.)--Biomedical Engineering, Georgia Institute of Technology, 2007.
Committee Chair: Hu, Xiaoping; Committee Member: Brummer, Marijn; Committee Member: Butera, Robert; Committee Member: Oshinski, John; Committee Member: Sathian, Krish.
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6

Stephens, Alexandre, and N/A. "Genetic and Functional Characterization of RUNX2." Griffith University. School of Medical Science, 2007. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070823.100953.

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RUNX2 belongs to the RUNT domain family of transcription factors of which three have been identified in humans (RUNX1, RUNX2 and RUNX3). RUNX proteins are vital for metazoan development and participate in the regulation of cellular differentiation and cell cycle progression (Coffman, 2003). RUNX2 is required for proper bone formation by driving the differentiation of osteoblasts from mesenchymal progenitors during development (Ducy et al, 1997; Komori et al, 1997; Otto et al, 1997). RUNX2 is also vital for chondrocyte maturation by promoting the differentiation of chondrocytes to the hypertrophic phenotype (Enomoto et al, 2000). The consequences of completely disrupting the RUNX2 locus in mice provided compelling and conclusive evidence for the biological importance of RUNX2 where knockout mice died shortly after birth with a complete lack of bone formation (Komori et al, 1997; Otto et al, 1997). A further indication of the requisite role of RUNX2 in skeletal development was the discovery that RUNX2 haploinsufficiency in humans and mice caused the skeletal syndrome Cleidocranial Dysplasia (CCD) (Mundlos et al, 1997; Lee et al, 1997). A unique feature of RUNX2 is the consecutive polyglutamine and polyalanine tracts (Q/A domain). Mutations causing CCD have been observed in the Q/A domain of RUNX2 (Mundlos et al, 1997). The Q/A domain is an essential part of RUNX2 and participates in transactivation function (Thirunavukkarasu et al, 1998). Previous genotyping studies conducted in our laboratory identified several rare RUNX2 Q/A variants in addition to a frequently occurring 18 base pair deletion of the polyalanine tract termed the 11Ala allele. Analysis of serum parameters in 78 Osteoarthritis patients revealed the 11Ala allele was associated with significantly decreased osteocalcin. Furthermore, analysis of 11Ala allele frequencies within a Geelong Osteoporosis Study (GOS) fracture cohort and an appropriate age matched control group revealed the 11Ala allele was significantly overrepresented in fracture cases indicating an association with increased fracture risk. To further investigate the 11Ala allele and rare Q/A variants, 747 DNA samples from the Southeast Queensland bone study were genotyped using PCR and PAGE. The experiment served two purposes: 1) to detect additional rare Q/A variants to enrich the population of already identified mutants and 2) have an independent assessment of the effect of the 11Ala allele on fracture to either support or refute our previous observation which indicated the 11Ala allele was associated with an increased risk of fracture in the GOS. From the 747 samples genotyped, 665 were WT, 76 were heterozygous for the 11Ala allele, 5 were homozygous for the 11Ala allele and 1 was heterozygous for a rare 21 bp deletion of the polyglutamine tract. Chi-square analysis of RUNX2 genotype distributions within fracture and non-fracture groups in the Southeast Queensland bone study revealed that individuals that carried at least one copy of the 11Ala allele were enriched in the fracture group (p = 0.16, OR = 1.712). The OR of 1.712 was of similar magnitude to the OR observed in the GOS case-control investigation (OR = 1.9) providing support for the original study. Monte-Carlo simulations were used to combine the results from the GOS and the Southeast Queensland bone study. The simulations were conducted with 10000 iterations and demonstrated that the maximum probability of obtaining both study results by chance was less than 5 times in two hundred (p < 0.025) suggesting that the 11Ala allele of RUNX2 was associated with an increased fracture risk. The second element of the research involved the analysis of rare RUNX2 Q/A variants identified from multiple epidemiological studies of bone. Q/A repeat variants were derived from four populations: the GOS, an Aberdeen cohort, CAIFOS and a Sydney twin study. Collectively, a total of 20 rare glutamine and one alanine variants were identified from 4361 subjects. All RUNX2 Q/A variants were heterozygous for a mutant allele and a wild type allele. Analysis of incident fracture during a five year follow up period in the CAIFOS revealed that Q-variants (n = 8) were significantly more likely to have fractured compared to non-carriers (p = 0.026, OR 4.932 95% CI 1.2 to 20.1). Bone density data as measured by quantitative ultrasound was available for CAIFOS. Analysis of BUA and SOS Z-scores revealed that Q-repeat variants had significantly lower BUA (p = 0.031, mean Z-score of -0.79) and a trend for lower SOS (p = 0.190, mean Z-score of -0.69). BMD data was available for all four populations. To normalize the data across the four studies, FN BMD data was converted into Z-scores and the effect of the Q/A variants on BMD was analysed using a one sample approach. The analysis revealed Q/A variants had significantly lower FN BMD (p = 0.0003) presenting with a 0.65 SD decrease. Quantitative transactivation analysis was conducted on RUNX2 proteins harbouring rare glutamine mutations and the 11Ala allele. RUNX2 proteins containing a glutamine deletion (16Q), a glutamine insertion (30Q) and the 11Ala allele were overexpressed in NIH3T3 and HEK293 cells and their ability to transactivate a known target promoter was assessed. The 16Q and 30Q had significantly decreased reporter activity compared to WT in NIH3T3 cells (p = 0.002 and 0.016, for 16Q and 30Q, respectively). In contrast 11Ala RUNX2 did not show significantly different promoter activation potential (p = 0.54). Similar results were obtained in HEK293 cells where both the 16Q and 30Q RUNX2 displayed decreased reporter activity (p=0.007 and 0.066 for 16Q and 30Q respectively) whereas the 11Ala allele had no material effect on RUNX2 function (p = 0.20). The RUNX2 gene target reporter assay provided evidence to suggest that variation within the glutamine tract of RUNX2 was capable of altering the ability of RUNX2 to activate a known target promoter. In contrast, the 11Ala allele showed no variation in RUNX2 activity. The third feature of the research served the purpose of identifying potential RUNX2 gene targets with particular emphasis on discovering genes cooperatively regulated by RUNX2 and the powerful bone promoting agent BMP2. The experiment was conducted by creating stably transfected NIH3T3 cells lines overexpressing RUNX2 or BMP2 or both RUNX2 and BMP2. Microarray analysis revealed very few genes were differentially regulated between standard NIH3T3 cells and cells overexpressing RUNX2. The results were confirmed via RT-PCR analysis which demonstrated that the known RUNX2 gene targets Osteocalcin and Matrix Metalloproteinase-13 were modestly induced 2.5 fold (p = 0.00017) and 2.1 fold (p = 0.002) respectively in addition to identifying only two genes (IGF-II and SCYA11) that were differentially regulated greater than 10 fold. IGF-II and SYCA11 were significantly down-regulated 27.6 fold (p = 1.95 x 10-6) and 10.1 fold (p = 0.0002) respectively. The results provided support for the notion that RUNX2 on its own was not sufficient for optimal gene expression and required the presence of additional factors. To discover genes cooperatively regulated by RUNX2 and BMP2, microarray gene expression analysis was performed on standard NIH3T3 cells and NIH3T3 cells stably transfected with both RUNX2 and BMP2. Comparison of the gene expression profiles revealed the presence of a large number of differentially regulated genes. Four genes EHOX, CCL9, CSF2 and OSF-1 were chosen to be further characterized via RT-PCR. Sequential RT-PCR analysis on cDNA derived from control cells and cells stably transfected with either RUNX2, BMP2 or both RUNX2/BMP2 revealed that EHOX and CSF2 were cooperatively induced by RUNX2 and BMP2 whereas CCL9 and OSF-1 were suppressed by BMP2. The overexpression of both RUNX2 and BMP2 in NIH3T3 fibroblasts provided a powerful model upon which to discover potential RUNX2 gene targets and also identify genes synergistically regulated by BMP2 and RUNX2. The fourth element of the research investigated the role of RUNX2 in the ascorbic acid mediated induction of MMP-13 mRNA. The study was carried out using NIH3T3 cell lines stably transfected with BMP2, RUNX2 and both BMP2 and RUNX2. The cell lines were grown to confluence and subsequently cultured for a further 12 days in standard media or in media supplemented with AA. RT-PCR analysis was used to assess MMP-13 mRNA expression. The RT-PCR results demonstrated that AA was not sufficient for inducing MMP-13 mRNA in NIH3T3 cells. In contrast RUNX2 significantly induced MMP-13 levels 85 fold in the absence of AA (p = 0.0055) and upregulated MMP-13 mRNA levels 254 fold in the presence of AA (p = 0.0017). The results demonstrated that RUNX2 was essential for the AA mediated induction of MMP-13 mRNA in NIH3T3 cells. The effect of BMP2 on MMP-13 expression was also investigated. BMP2 induced MMP-13 mRNA transcripts a modest 3.8 fold in the presence of AA (p = 0.0027). When both RUNX2 and BMP2 were overexpressed in the presence of AA, MMP-13 mRNA levels were induced a massive 4026 fold (p = 8.7 x 10-4) compared to control cells. The investigation revealed that RUNX2 was an essential factor for the AA mediated induction of MMP-13 and that RUNX2 and BMP2 functionally cooperated to regulate MMP-13 mRNA levels.
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7

Stephens, Alexandre. "Genetic and Functional Characterization of RUNX2." Thesis, Griffith University, 2007. http://hdl.handle.net/10072/365677.

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RUNX2 belongs to the RUNT domain family of transcription factors of which three have been identified in humans (RUNX1, RUNX2 and RUNX3). RUNX proteins are vital for metazoan development and participate in the regulation of cellular differentiation and cell cycle progression (Coffman, 2003). RUNX2 is required for proper bone formation by driving the differentiation of osteoblasts from mesenchymal progenitors during development (Ducy et al, 1997; Komori et al, 1997; Otto et al, 1997). RUNX2 is also vital for chondrocyte maturation by promoting the differentiation of chondrocytes to the hypertrophic phenotype (Enomoto et al, 2000). The consequences of completely disrupting the RUNX2 locus in mice provided compelling and conclusive evidence for the biological importance of RUNX2 where knockout mice died shortly after birth with a complete lack of bone formation (Komori et al, 1997; Otto et al, 1997). A further indication of the requisite role of RUNX2 in skeletal development was the discovery that RUNX2 haploinsufficiency in humans and mice caused the skeletal syndrome Cleidocranial Dysplasia (CCD) (Mundlos et al, 1997; Lee et al, 1997). A unique feature of RUNX2 is the consecutive polyglutamine and polyalanine tracts (Q/A domain). Mutations causing CCD have been observed in the Q/A domain of RUNX2 (Mundlos et al, 1997). The Q/A domain is an essential part of RUNX2 and participates in transactivation function (Thirunavukkarasu et al, 1998). Previous genotyping studies conducted in our laboratory identified several rare RUNX2 Q/A variants in addition to a frequently occurring 18 base pair deletion of the polyalanine tract termed the 11Ala allele. Analysis of serum parameters in 78 Osteoarthritis patients revealed the 11Ala allele was associated with significantly decreased osteocalcin. Furthermore, analysis of 11Ala allele frequencies within a Geelong Osteoporosis Study (GOS) fracture cohort and an appropriate age matched control group revealed the 11Ala allele was significantly overrepresented in fracture cases indicating an association with increased fracture risk. To further investigate the 11Ala allele and rare Q/A variants, 747 DNA samples from the Southeast Queensland bone study were genotyped using PCR and PAGE. The experiment served two purposes: 1) to detect additional rare Q/A variants to enrich the population of already identified mutants and 2) have an independent assessment of the effect of the 11Ala allele on fracture to either support or refute our previous observation which indicated the 11Ala allele was associated with an increased risk of fracture in the GOS. From the 747 samples genotyped, 665 were WT, 76 were heterozygous for the 11Ala allele, 5 were homozygous for the 11Ala allele and 1 was heterozygous for a rare 21 bp deletion of the polyglutamine tract. Chi-square analysis of RUNX2 genotype distributions within fracture and non-fracture groups in the Southeast Queensland bone study revealed that individuals that carried at least one copy of the 11Ala allele were enriched in the fracture group (p = 0.16, OR = 1.712). The OR of 1.712 was of similar magnitude to the OR observed in the GOS case-control investigation (OR = 1.9) providing support for the original study. Monte-Carlo simulations were used to combine the results from the GOS and the Southeast Queensland bone study. The simulations were conducted with 10000 iterations and demonstrated that the maximum probability of obtaining both study results by chance was less than 5 times in two hundred (p < 0.025) suggesting that the 11Ala allele of RUNX2 was associated with an increased fracture risk. The second element of the research involved the analysis of rare RUNX2 Q/A variants identified from multiple epidemiological studies of bone. Q/A repeat variants were derived from four populations: the GOS, an Aberdeen cohort, CAIFOS and a Sydney twin study. Collectively, a total of 20 rare glutamine and one alanine variants were identified from 4361 subjects. All RUNX2 Q/A variants were heterozygous for a mutant allele and a wild type allele. Analysis of incident fracture during a five year follow up period in the CAIFOS revealed that Q-variants (n = 8) were significantly more likely to have fractured compared to non-carriers (p = 0.026, OR 4.932 95% CI 1.2 to 20.1). Bone density data as measured by quantitative ultrasound was available for CAIFOS. Analysis of BUA and SOS Z-scores revealed that Q-repeat variants had significantly lower BUA (p = 0.031, mean Z-score of -0.79) and a trend for lower SOS (p = 0.190, mean Z-score of -0.69). BMD data was available for all four populations. To normalize the data across the four studies, FN BMD data was converted into Z-scores and the effect of the Q/A variants on BMD was analysed using a one sample approach. The analysis revealed Q/A variants had significantly lower FN BMD (p = 0.0003) presenting with a 0.65 SD decrease. Quantitative transactivation analysis was conducted on RUNX2 proteins harbouring rare glutamine mutations and the 11Ala allele. RUNX2 proteins containing a glutamine deletion (16Q), a glutamine insertion (30Q) and the 11Ala allele were overexpressed in NIH3T3 and HEK293 cells and their ability to transactivate a known target promoter was assessed. The 16Q and 30Q had significantly decreased reporter activity compared to WT in NIH3T3 cells (p = 0.002 and 0.016, for 16Q and 30Q, respectively). In contrast 11Ala RUNX2 did not show significantly different promoter activation potential (p = 0.54). Similar results were obtained in HEK293 cells where both the 16Q and 30Q RUNX2 displayed decreased reporter activity (p=0.007 and 0.066 for 16Q and 30Q respectively) whereas the 11Ala allele had no material effect on RUNX2 function (p = 0.20). The RUNX2 gene target reporter assay provided evidence to suggest that variation within the glutamine tract of RUNX2 was capable of altering the ability of RUNX2 to activate a known target promoter. In contrast, the 11Ala allele showed no variation in RUNX2 activity. The third feature of the research served the purpose of identifying potential RUNX2 gene targets with particular emphasis on discovering genes cooperatively regulated by RUNX2 and the powerful bone promoting agent BMP2. The experiment was conducted by creating stably transfected NIH3T3 cells lines overexpressing RUNX2 or BMP2 or both RUNX2 and BMP2. Microarray analysis revealed very few genes were differentially regulated between standard NIH3T3 cells and cells overexpressing RUNX2. The results were confirmed via RT-PCR analysis which demonstrated that the known RUNX2 gene targets Osteocalcin and Matrix Metalloproteinase-13 were modestly induced 2.5 fold (p = 0.00017) and 2.1 fold (p = 0.002) respectively in addition to identifying only two genes (IGF-II and SCYA11) that were differentially regulated greater than 10 fold. IGF-II and SYCA11 were significantly down-regulated 27.6 fold (p = 1.95 x 10-6) and 10.1 fold (p = 0.0002) respectively. The results provided support for the notion that RUNX2 on its own was not sufficient for optimal gene expression and required the presence of additional factors. To discover genes cooperatively regulated by RUNX2 and BMP2, microarray gene expression analysis was performed on standard NIH3T3 cells and NIH3T3 cells stably transfected with both RUNX2 and BMP2. Comparison of the gene expression profiles revealed the presence of a large number of differentially regulated genes. Four genes EHOX, CCL9, CSF2 and OSF-1 were chosen to be further characterized via RT-PCR. Sequential RT-PCR analysis on cDNA derived from control cells and cells stably transfected with either RUNX2, BMP2 or both RUNX2/BMP2 revealed that EHOX and CSF2 were cooperatively induced by RUNX2 and BMP2 whereas CCL9 and OSF-1 were suppressed by BMP2. The overexpression of both RUNX2 and BMP2 in NIH3T3 fibroblasts provided a powerful model upon which to discover potential RUNX2 gene targets and also identify genes synergistically regulated by BMP2 and RUNX2. The fourth element of the research investigated the role of RUNX2 in the ascorbic acid mediated induction of MMP-13 mRNA. The study was carried out using NIH3T3 cell lines stably transfected with BMP2, RUNX2 and both BMP2 and RUNX2. The cell lines were grown to confluence and subsequently cultured for a further 12 days in standard media or in media supplemented with AA. RT-PCR analysis was used to assess MMP-13 mRNA expression. The RT-PCR results demonstrated that AA was not sufficient for inducing MMP-13 mRNA in NIH3T3 cells. In contrast RUNX2 significantly induced MMP-13 levels 85 fold in the absence of AA (p = 0.0055) and upregulated MMP-13 mRNA levels 254 fold in the presence of AA (p = 0.0017). The results demonstrated that RUNX2 was essential for the AA mediated induction of MMP-13 mRNA in NIH3T3 cells. The effect of BMP2 on MMP-13 expression was also investigated. BMP2 induced MMP-13 mRNA transcripts a modest 3.8 fold in the presence of AA (p = 0.0027). When both RUNX2 and BMP2 were overexpressed in the presence of AA, MMP-13 mRNA levels were induced a massive 4026 fold (p = 8.7 x 10-4) compared to control cells. The investigation revealed that RUNX2 was an essential factor for the AA mediated induction of MMP-13 and that RUNX2 and BMP2 functionally cooperated to regulate MMP-13 mRNA levels.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Faculty of Health
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8

Smoler, Gunilla Kanter. "Functional characterization of conserved checkpoint genes." Göteborg, Sweden : Dept. of Cellular and Molecular Biology, Göteborg University, 1998. http://books.google.com/books?id=vM5qAAAAMAAJ.

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Harris, Nicole L. "Functional characterization of recombinant bone sialoprotein." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ28580.pdf.

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Crimmins, Stephen Lewis. "Characterization and functional analysis of Usp14." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2007p/crimmins.pdf.

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Books on the topic "Functional Characterization"

1

Matheson, Kimberly. Functional characterization of the RHD promoter. Ottawa: National Library of Canada, 2002.

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Huber, Eva Maria. Structural and Functional Characterization of the Immunoproteasome. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-01556-9.

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A, Favre Eduardo, and Fuentes Néstor O, eds. Functional properties of bio-inspired surfaces: Characterization and technological applications. Hackensack, NJ: World Scientific, 2009.

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Functional equations and characterization problems on locally compact Abelian groups. Zurich: European Mathematical Society, 2008.

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Randhawa, Varinder K. Functional characterization of vesicle-snares in GLUT4 glucose transporter vesicle traffic. Ottawa: National Library of Canada, 2002.

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Walz, Bernd. Calcium-sequestering cell organelles: In situ localization, morphological and functional characterization. Stuttgart: G. Fischer, 1989.

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I, Kingon Angus, Vilarinho Paula Maria, and Rosenwaks Yossi, eds. Scanning probe microscopy: Characterization, nanofabrication and device application of functional materials. Dordrecht: Kluwer Academic Publishers, 2005.

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Roepke, Jonathon. Localization and functional characterization of iridoid biosynthetic genes in Catharanthus roseus. St. Catharines, Ont: Brock University, Centre for Biotechnology, 2008.

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Vilarinho, Paula Maria, Yossi Rosenwaks, and Angus Kingon, eds. Scanning Probe Microscopy: Characterization, Nanofabrication and Device Application of Functional Materials. Dordrecht: Springer Netherlands, 2005. http://dx.doi.org/10.1007/1-4020-3019-3.

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Sanyal, Suparna. Pharmacological and functional characterization of the polymorphic human dopamine D4 receptor isoforms. Ottawa: National Library of Canada, 1996.

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Book chapters on the topic "Functional Characterization"

1

Myers, Chester. "Functional Attributes of Protein Isolates." In Characterization of Proteins, 491–549. Totowa, NJ: Humana Press, 1988. http://dx.doi.org/10.1007/978-1-59259-437-5_19.

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D’Ambrosio, Bruce. "Characterization of Functional Relationships." In Qualitative Process Theory Using Linguistic Variables, 96–119. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4613-9671-0_8.

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Kumar, Sarita, Aarti Sharma, Drashya Gautam, and Sunita Hooda. "Characterization of Mesoporous Materials." In Advanced Functional Porous Materials, 175–204. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-85397-6_6.

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Somo, Thabang R., Mpitloane J. Hato, and Kwena D. Modibane. "Characterization of Macroporous Materials." In Advanced Functional Porous Materials, 87–111. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-85397-6_4.

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Keshavarz, Leila, Mohammad Reza Ghaani, Omid Saremi, and Niall J. English. "Characterization of Nanoporous Materials." In Advanced Functional Porous Materials, 319–51. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-85397-6_10.

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Lillford, Peter J. "Characterization and Functional Attributes of Protein Isolates." In Characterization of Proteins, 467–90. Totowa, NJ: Humana Press, 1988. http://dx.doi.org/10.1007/978-1-59259-437-5_18.

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Tikekar, Rohan V. "Characterization of nanoscale delivery systems." In Nanotechnology and Functional Foods, 112–29. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118462157.ch7.

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Hu, Haijing, Matthew M. Moake, Abigail B. Snyder, and Randy W. Worobo. "Genetic Characterization of Antimicrobial Peptides." In Functional Foods and Biotechnology, 379–406. Boca Raton : CRC Press, [2020] | Series: Food biotechnology: CRC Press, 2020. http://dx.doi.org/10.1201/9781003003793-22.

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Azam, Mohd Asyadi, Nur Ezyanie Safie, and Mohd Fareezuan Abdul Aziz. "Characterization of Hierarchical Porous Materials." In Advanced Functional Porous Materials, 407–29. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-85397-6_13.

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Selby, David S., Martin R. Larsen, Cosima Damiana Calvano, and Ole Nørregaard Jensen. "Identification and Characterization of N-Glycosylated Proteins Using Proteomics." In Functional Proteomics, 263–76. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-398-1_17.

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Conference papers on the topic "Functional Characterization"

1

Parmar, R. J., V. R. Solanki, R. J. Pathak, and M. D. Parmar. "Synthesis and characterization of tin sulfide nanoparticles." In FUNCTIONAL OXIDES AND NANOMATERIALS: Proceedings of the International Conference on Functional Oxides and Nanomaterials. Author(s), 2017. http://dx.doi.org/10.1063/1.4982107.

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Dumasiya, Ajay, and N. M. Shah. "Solvothermal synthesis and characterization of CZTS nanocrystals." In FUNCTIONAL OXIDES AND NANOMATERIALS: Proceedings of the International Conference on Functional Oxides and Nanomaterials. Author(s), 2017. http://dx.doi.org/10.1063/1.4982151.

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Obrzut, Jan. "Interconnection continuity test for packaged functional modules." In CHARACTERIZATION AND METROLOGY FOR ULSI TECHNOLOGY. ASCE, 1998. http://dx.doi.org/10.1063/1.56914.

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Shah, N. M., and K. C. Poria. "Structural and optical characterization of bismuth sulphide nanorods." In FUNCTIONAL OXIDES AND NANOMATERIALS: Proceedings of the International Conference on Functional Oxides and Nanomaterials. Author(s), 2017. http://dx.doi.org/10.1063/1.4982153.

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Tank, Nirali S., K. D. Parikh, and M. J. Joshi. "Synthesis and characterization of copper sulphide (CuS) nano particles." In FUNCTIONAL OXIDES AND NANOMATERIALS: Proceedings of the International Conference on Functional Oxides and Nanomaterials. Author(s), 2017. http://dx.doi.org/10.1063/1.4982102.

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De, Manojit, Ananya Rout, and H. S. Tewari. "Synthesis and structural characterization of A-site doped NiFe2O4." In FUNCTIONAL OXIDES AND NANOMATERIALS: Proceedings of the International Conference on Functional Oxides and Nanomaterials. Author(s), 2017. http://dx.doi.org/10.1063/1.4982126.

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Mallick, P., C. S. Sahoo, and N. C. Mishra. "Structural and optical characterization of NiO nanoparticles synthesized by sol-gel route." In FUNCTIONAL MATERIALS: Proceedings of the International Workshop on Functional Materials (IWFM-2011). AIP, 2012. http://dx.doi.org/10.1063/1.4736893.

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Tseng, Ming Lun, Aleksandrs l. Leitis, Aurelian John-Herpin, Yuri S. Kivshar, and Hatice Altug. "Wafer-scale nanofabrication of functional metasurfaces." In Plasmonics: Design, Materials, Fabrication, Characterization, and Applications XX, edited by Yu-Jung Lu, Takuo Tanaka, and Din Ping Tsai. SPIE, 2022. http://dx.doi.org/10.1117/12.2632574.

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Panda, P. K. "Development of PZT materials, fabrication and characterization of multi layered actuators for aerospace applications." In FUNCTIONAL MATERIALS: Proceedings of the International Workshop on Functional Materials (IWFM-2011). AIP, 2012. http://dx.doi.org/10.1063/1.4736880.

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Yang, Xu, Chao Geng, Xiaoyang Li, Bincheng Li, and Xinyang Li. "Characterization of Kepler structured microlens array scanners for 2D scanning." In Novel Optoelectronic Functional Materials and Devices, edited by Xiong Li, Zhuo Xu, Mingbo Pu, Costas Fotakis, Xiangang Luo, and Xiaoliang Ma. SPIE, 2021. http://dx.doi.org/10.1117/12.2603968.

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Reports on the topic "Functional Characterization"

1

Wilson, D. M. III. Functional characterization of dna repair proteins. Office of Scientific and Technical Information (OSTI), February 2000. http://dx.doi.org/10.2172/15001995.

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Straalsund, E. K. Gas characterization system functional design criteria. Office of Scientific and Technical Information (OSTI), January 1995. http://dx.doi.org/10.2172/10116382.

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Schneider, T. C. Gas characterization monitoring system functional design criteria. Office of Scientific and Technical Information (OSTI), June 1997. http://dx.doi.org/10.2172/325281.

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Tate, D. D. Functional requirements for gas characterization system computer software. Office of Scientific and Technical Information (OSTI), January 1996. http://dx.doi.org/10.2172/470869.

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Nelson, Tammie. DFT for design and characterization of functional materials. Office of Scientific and Technical Information (OSTI), March 2021. http://dx.doi.org/10.2172/1772398.

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Lue, Neal F. Structural and Functional Characterization of a Telomerase-Associated Endonuclease. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada411390.

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Lue, Neal F. Structural and Functional Characterization of a Telomerase-Associated Endonuclease. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada417028.

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Couch, Fergus J. Characterization of BRCA2 Mutation in a Series of Functional Assays. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada437782.

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Couch, Fergus J. Characterization of BRCA2 Mutations in a Series of Functional Assays. Fort Belvoir, VA: Defense Technical Information Center, May 2001. http://dx.doi.org/10.21236/ada395843.

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Abdel-Mageed, Asim B., Krishna C. Agrawal, Jr Crawford, and Byron. Functional Characterization of Two Novel Human Prostate Cancer Metastasis Related Genes. Fort Belvoir, VA: Defense Technical Information Center, February 2008. http://dx.doi.org/10.21236/ada493881.

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