Relevant bibliographies by topics / ACTN1

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'ACTN1'

Author: Grafiati
Published: 1 April 2023

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Journal articles on the topic "ACTN1"

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Boutroux, Helene, Bianca David, Paul Guéguen, Pierre Frange, Anne Vincenot, Guy Leverger, and Rémi Favier. "ACTN1-related Macrothrombocytopenia." Journal of Pediatric Hematology/Oncology 39, no. 8 (November 2017): e515-e518. http://dx.doi.org/10.1097/mph.0000000000000885.

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Bottega, Roberta, Caterina Marconi, Michela Faleschini, Gabriele Baj, Claudia Cagioni, Alessandro Pecci, Tommaso Pippucci, et al. "ACTN1-related thrombocytopenia: identification of novel families for phenotypic characterization." Blood 125, no. 5 (January 29, 2015): 869–72. http://dx.doi.org/10.1182/blood-2014-08-594531.

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Key Points ACTN1 mutations were identified in 10 of 239 families with inherited thrombocytopenia of unknown origin. ACTN1-related thrombocytopenia is characterized by mild thrombocytopenia with platelet macrocytosis and low risk for bleeding.
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Dubayle, David, Arnaud Vanden-Bossche, Tom Peixoto, and Jean-Luc Morel. "Hypergravity Increases Blood–Brain Barrier Permeability to Fluorescent Dextran and Antisense Oligonucleotide in Mice." Cells 12, no. 5 (February 24, 2023): 734. http://dx.doi.org/10.3390/cells12050734.

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The earliest effect of spaceflight is an alteration in vestibular function due to microgravity. Hypergravity exposure induced by centrifugation is also able to provoke motion sickness. The blood–brain barrier (BBB) is the crucial interface between the vascular system and the brain to ensure efficient neuronal activity. We developed experimental protocols of hypergravity on C57Bl/6JRJ mice to induce motion sickness and reveal its effects on the BBB. Mice were centrifuged at 2× g for 24 h. Fluorescent dextrans with different sizes (40, 70 and 150 kDa) and fluorescent antisense oligonucleotides (AS) were injected into mice retro-orbitally. The presence of fluorescent molecules was revealed by epifluorescence and confocal microscopies in brain slices. Gene expression was evaluated by RT-qPCR from brain extracts. Only the 70 kDa dextran and AS were detected in the parenchyma of several brain regions, suggesting an alteration in the BBB. Moreover, Ctnnd1, Gja4 and Actn1 were upregulated, whereas Jup, Tjp2, Gja1, Actn2, Actn4, Cdh2 and Ocln genes were downregulated, specifically suggesting a dysregulation in the tight junctions of endothelial cells forming the BBB. Our results confirm the alteration in the BBB after a short period of hypergravity exposure.
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Kunishima, Shinji, Katsumasa Kitamura, Motoko Yasutomi, and Ryoji Kobayashi. "Diagnostic biomarker for ACTN1 macrothrombocytopenia." Blood 126, no. 22 (November 26, 2015): 2525–26. http://dx.doi.org/10.1182/blood-2015-08-666180.

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Westbury, Sarah K., Deborah K. Shoemark, and Andrew D. Mumford. "ACTN1 variants associated with thrombocytopenia." Platelets 28, no. 6 (August 18, 2017): 625–27. http://dx.doi.org/10.1080/09537104.2017.1356455.

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Kunishima, Shinji, Yusuke Okuno, Kenichi Yoshida, Yuichi Shiraishi, Masashi Sanada, Hideki Muramatsu, Kenichi Chiba, et al. "ACTN1 Mutations Cause Congenital Macrothrombocytopenia." American Journal of Human Genetics 92, no. 3 (March 2013): 431–38. http://dx.doi.org/10.1016/j.ajhg.2013.01.015.

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Yang, Xinrui, Yifan Pang, Jilei Zhang, Jinlong Shi, Xinpei Zhang, Gaoqi Zhang, Siyuan Yang, et al. "High Expression Levels of ACTN1 and ACTN3 Indicate Unfavorable Prognosis in Acute Myeloid Leukemia." Journal of Cancer 10, no. 18 (2019): 4286–92. http://dx.doi.org/10.7150/jca.31766.

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Suresh, Rahul, Sophie Fiola, Jamie Beaulieu, and Roberto Diaz. "PATH-14. ALPHA CARDIAC ACTIN EXPRESSION IS OBSERVED IN AGGRESSIVE GLIOMA SUBTYPES AND GLIOBLASTOMA STEM CELLS." Neuro-Oncology 23, Supplement_6 (November 2, 2021): vi117. http://dx.doi.org/10.1093/neuonc/noab196.466.

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Abstract BACKGROUND Alterations in actin subunit expression have previously been observed in multiple cancers. In glioblastoma (GBM), the expression of ACTC1 has been associated with a more invasive phenotype and with shorter survival. We sought to explore the diversity of actin subunit expression across glioma subtypes and patient derived glioblastoma stem cells (GSCs). METHODS Bioinformatic analysis of multiple glioma databases was performed to profile actin subunit (ACTA1, ACTA2, ACTC1, ACTG1, ACTG2, and ACTB) mRNA levels. Expression levels were also evaluated in normal brain in comparison to liver and heart tissue. Western blot was used to analyze protein expression in GSCs, surgical tissue and human fetal astrocytes. RESULTS The primary actin subunits expressed in normal brain are beta actin (ACTB) and gamma actin (ACTG1). RNA sequencing of tissue from multiple glioma subtypes or different brain regions reveals a global increase in ACTG1 and ACTB abundance in gliomas compared to normal brain. LGG-GCIMP high and LGG-co-deleted glioma subtypes have the lowest ACTC1 expression. LGG-GCIMP low (HR 9.75, P< 0.001), LGG-mesenchymal-like (HR11.1, P< 0.001), LGG-classic-like (HR10.96, P< 0.001) subtypes are associated with ACTC1 expression. ACTC1, ACTCB, and ACTG protein expression was observed in GSCs, freshly resected GBM tissue, and human fetal astrocytes. CONCLUSIONS Gliomas have a specific pattern of actin subunit expression that differs in actin subunit type and abundance when compared to normal adult brain. Expression of ACTC1 is found in aggressive glioma subtypes and is shared by GSCs and human fetal astrocytes. Investigation into the neurodevelopmental role of ACTC1 and its contribution to oncogenic transformation in GBM is warranted.
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Vincenot, Anne, Paul Saultier, Shinji Kunishima, Marjorie Poggi, Marie‐Françoise Hurtaud‐Roux, Alain Roussel, ACTN1 study coinvestigators, Nicole Schlegel, and Marie‐Christine Alessi. "Novel ACTN1 variants in cases of thrombocytopenia." Human Mutation 40, no. 12 (November 6, 2019): 2258–69. http://dx.doi.org/10.1002/humu.23840.

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Ashaie, Maeirah Afzal, Rowshan Ara Islam, Nur Izyani Kamaruzman, Nabilah Ibnat, Kyi Kyi Tha, and Ezharul Hoque Chowdhury. "Targeting Cell Adhesion Molecules via Carbonate Apatite-Mediated Delivery of Specific siRNAs to Breast Cancer Cells In Vitro and In Vivo." Pharmaceutics 11, no. 7 (July 2, 2019): 309. http://dx.doi.org/10.3390/pharmaceutics11070309.

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While several treatment strategies are applied to cure breast cancer, it still remains one of the leading causes of female deaths worldwide. Since chemotherapeutic drugs have severe side effects and are responsible for development of drug resistance in cancer cells, gene therapy is now considered as one of the promising options to address the current treatment limitations. Identification of the over-expressed genes accounting for constitutive activation of certain pathways, and their subsequent knockdown with specific small interfering RNAs (siRNAs), could be a powerful tool in inhibiting proliferation and survival of cancer cells. In this study, we delivered siRNAs against mRNA transcripts of over-regulated cell adhesion molecules such as catenin alpha 1 (CTNNA1), catenin beta 1 (CTNNB1), talin-1 (TLN1), vinculin (VCL), paxillin (PXN), and actinin-1 (ACTN1) in human (MCF-7 and MDA-MB-231) and murine (4T1) cell lines as well as in the murine female Balb/c mice model. In order to overcome the barriers of cell permeability and nuclease-mediated degradation, the pH-sensitive carbonate apatite (CA) nanocarrier was used as a delivery vehicle. While targeting CTNNA1, CTNNB1, TLN1, VCL, PXN, and ACTN1 resulted in a reduction of cell viability in MCF-7 and MDA-MB-231 cells, delivery of all these siRNAs via carbonate apatite (CA) nanoparticles successfully reduced the cell viability in 4T1 cells. In 4T1 cells, delivery of CTNNA1, CTNNB1, TLN1, VCL, PXN, and ACTN1 siRNAs with CA caused significant reduction in phosphorylated and total AKT levels. Furthermore, reduced band intensity was observed for phosphorylated and total MAPK upon transfection of 4T1 cells with CTNNA1, CTNNB1, and VCL siRNAs. Intravenous delivery of CTNNA1 siRNA with CA nanoparticles significantly reduced tumor volume in the initial phase of the study, while siRNAs targeting CTNNB1, TLN1, VCL, PXN, and ACTN1 genes significantly decreased the tumor burden at all time points. The tumor weights at the end of the treatments were also notably smaller compared to CA. This successfully demonstrates that targeting these dysregulated genes via RNAi and by using a suitable delivery vehicle such as CA could serve as a promising therapeutic treatment modality for breast cancers.
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Dissertations / Theses on the topic "ACTN1"

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Zablocki, Destinee Elizabeth. "Differential Expression of Calsarcin Genes in Orthognathic Surgery Patients with ACTN3 R577X Gene Deviations." Master's thesis, Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/405298.

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Oral Biology
M.S.
Objective: Malocclusion is a complex musculoskeletal trait, with muscle playing an integral role in vertical facial development. A single nucleotide polymorphism (SNP) produces the R577XX nonsense mutation in the alpha-actinin-3 (ACTN3) gene, creating a stop codon and loss of its protein. With loss of ACTN3, alpha-actinin-2 (ACTN2) is upregulated. Calsarcins, known inhibitors of calcineurin activation, preferentially bind ACTN2 leading to a surge in free calcineurin. The increase in calcineurin activity produces the phenotypic shift of fast muscle fibers toward the slow myogenic program seen in the ACTN3 null genotype (Seto et al., 2013). Here, we have tested whether calsarcin gene expression is affected by ACTN3 genotypes in human masseter muscle. Methods: Subjects undergoing orthodontic treatment and orthognathic surgery were recruited from the University of Lille, Department of Oral and Maxillofacial Surgery in Northern France. During the bilateral sagittal split osteotomy, masseter muscle samples were collected from the discarded section of deep anterior superficial masseter muscle, snap frozen, and shipped to Dr. Sciote’s lab at Temple University. RNA from masseter muscle samples was isolated from 41 subjects using TRIzolTM reagent. MYOZ gene expression was quantified by RT-PCR using an adult skeletal muscle reference standard (commercially prepared skeletal muscle RNA; Ambion, Inc), and individual primer-probe sets for MYOZ1, MYOZ2, MYOZ3, and HPRT1 (utilized for normalization of data). ANOVA and unpaired t-tests were used to determine the significance of expression differences between MYOZ genes and by ACTN3 R577X genotypes, as well as by malocclusion classes. Pearson analyses were used to determine correlations between MYOZ expression and fiber type mean percent occupancies. Results: The main aim of this project was to determine whether expression of the three calsarcin genes, MYOZ1, 2, and 3, differs between subjects with RR, RX and XX genotypes for the ACTN3 gene, as well as between sagittal and vertical classes of malocclusion, asymmetries and TMD. Differences were found for MYOZ3 expression where relative quantities in males, but not females, decreased progressively from the ACTN3 RR, to RX, and XX genotypes. Among subjects with the RX genotype, expression differed significantly between males and females by an unpaired t-test. A statistically significant difference was detected between MYOZ2 and Class II, Class III malocclusions (p=0.05). Sagittal differences were compared further by ANOVA analyses with a statistically significant difference detected for MYOZ3 with a probability of 0.02. Correlation analyses comparing fiber type mean % occupancy with calsarcin gene expression revealed a significant positive relationship between MYOZ2 and type I (slow-twitch) fibers. Correspondingly, a significant correlation of MYOZ2 expression with type IIA and IIX (fast-twitch) fibers was negative. Conclusions: The greatest relative quantity of RNA for the three calsarcin genes was found in MYOZ3, suggesting more calsarcin-3 may be needed in masticatory muscle structure and function than other calsarcin isoforms. Alternatively, high expression of MYOZ3 in the masseter samples may indicate that there are relatively greater amounts of that isoform in cranial muscle than in the limb skeletal muscle standard used in these studies. Also, relative quantities of MYOZ3 expression in males decreased progressively from the ACTN3 RR, to RX, and XX genotypes. While this data may suggest that the ACTN3 R577X polymorphism may affect MYOZ3 expression in males of the malocclusion patient population, an increased sample of male subjects would be needed to determine if this trend has true significance. Expression of MYOZ2 (calsarcin-1) was strongly correlated with slow fiber-type occupancy in masseter muscle of our patient population. The muscle-specific expression of each calsarcin may lend to the understanding of this result. MYOZ2 is the only isoform found in both cardiac muscle and slow-twitch skeletal muscle, while MYOZ1 and MYOZ3 are both found in skeletal muscle with a predilection towards fast-twitch skeletal muscle (Frey et al., 2004).
Temple University--Theses
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Zebrick, Brian Matthew. "ACTN3 R577X GENOTYPES ASSOCIATE WITH CLASS II AND DEEP BITE MALOCCLUSIONS." Master's thesis, Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/329277.

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Oral Biology
M.S.
Alpha-actinins are myofibril anchor proteins, which influence contractile properties of skeletal muscle. ACTN2 is expressed in slow type I and fast type II fibers whereas ACTN3 is expressed only in fast fibers. ACTN3 homozygosity for the 577X stop codon (i.e. changing 577RR to 577XX - the R577X polymorphism) results in the absence of alpha-actinin-3 in about 18% of Europeans, diminished fast contractile ability, enhanced endurance performance, and reduced bone mass or bone mineral density. We have examined ACTN3 expression and genetic variation in masseter muscle of orthognathic surgery patients to determine genotype associations with malocclusion. To determine the associations between genotypes and malocclusions, clinical information, masseter muscle biopsies, and saliva samples were obtained from 60 subjects. Genotyping for ACTN3 SNPs, RT-PCR quantitation of muscle gene message, and muscle morphometric fiber type properties were compared to determine statistical differences between genotype and phenotype. We found muscle mRNA expression level was significantly different for ACTN3 SNP genotypes (p<0.01). The frequency of ACTN3 genotypes was significantly different for sagittal and vertical classifications of malocclusion with the clearest association being elevated 577XX genotype in skeletal Class II malocclusion (p = 0.003). This genotype also resulted in significantly smaller diameter of fast type II fibers in masseter muscle (p=0.002). In conclusion, ACTN3 577XX is overrepresented in skeletal Class II malocclusion, suggesting a biologic influence during bone growth. ACTN3 577XX is underrepresented in deep bite malocclusion, suggesting muscle differences contribute to variations in vertical facial dimensions.
Temple University--Theses
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Nicholl, Sarah. "Characterisation of AAE7/ACN1 and aconitase isoforms from Arabidopsis thaliana." Thesis, Bangor University, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.536471.

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Hong, Lingzi. "Act1-Mediated RNA Metabolism in IL-17-Driven Inflammatory Diseases." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case162673878106271.

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Sniečkus, Audrius. "Raumenų pažaidos priklausomumas nuo krūvio išdėstymo strategijos, sportininkų specializacijos ir genotipo." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2013. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2013~D_20130610_125924-56862.

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Neįprasti didelio intensyvumo (ypač ekscentriniai) raumenų susitraukimai gali sukelti raumenų pažaidą (Yanagisawa et al., 2011; Neme et al., 2013), kuri pasireiškia sumažėjusia raumenų susitraukimo jėga Byrne et al., 2004; Skurvydas et al., 2010) miofibrilių Z linijos morfologiniais pokyčiais (Feasson et al., 2002), baltymų ištekėjimu iš pažeistų raumens skaidulų, raumenų skausmu, patinimu ir padidėjusiu standumu (Malisoux et al., 2006; Chen et al., 2013). Pažaida dažna pradėjus intensyviai treniruotis po santykinai mažo fizinio aktyvumo laikotarpio arba kaitant krūvio parametrus (intensyvumą, apimtį) siekiant išvengti monotonijos ir sukelti didžiausią adaptacinį atsaką (Bompa, 1999; Issurin, 2010). Ankstesniuose tyrimuose taikyti vienodo dydžio krūviai neatitinka sportinių pratybų specifiškumo (Nosaka, Clarkson, 1995; Chen, Hsieh, 2001): pratybose krūvio apimtis ir intensyvumas nuolatos keičiami, taikomos įvairios krūvio didinimo strategijos. Išlieka neaišku, kaip kinta raumenų pažaida ir motorinė funkcija didinant fizinį krūvį taikant skirtingas strategijas. Kėlėme hipotezę, kad: 1) nuosekliai didinamas krūvis sukelia mažesnę raumenų pažaidą, palyginti su staigiai didinamu krūviu, nes motorinė sistema labai jautriai reaguoja į krūvio didinimo greitį; 2) treniruotės ciklo metu periodiškai pasireiškianti didesnė raumenų pažaida dėl superkompensacijos gali sukelti didesnę ilgalaikę griaučių raumenų adaptaciją (masės ir jėgos prieaugį). R. Lynn ir D. L. Morgan (1994) nustatė... [toliau žr. visą tekstą]
Unaccustomed muscle exercise, especially when it involves high-strain eccentric contractions, causes muscle damage (Yanagisawa et al., 2011; Neme et al., 2013). Muscle damage manifests in altered Z-disk morphology (Feasson et al., 2002), prolonged impairment of muscle force (Byrne et al., 2004; Skurvydas et al., 2010), protein leakage from injured muscle fibres, delayed-onset muscle soreness, and increased passive muscle stiffness and swelling (Malisoux et al., 2006; Chen et al., 2013). Muscle damage is frequently induced by sports training, where physical load parameters are being varied on the temporal scale to avoid monotony and maximize the adaptations (Bompa 1999; Issurin, 2010). However, there are limited data on the development of muscle damage and its impact on muscle function when variant exercise training schemes are applied. More needs to be learned about the impact of different strategies of load increase on exercise-induced muscle damage in order to identify progression regimes that can optimize neuromuscular adaptation processes. Therefore, we have followed the dynamics of muscle function during the stretch–shortening exercise with differently increasing load. We increased training stimulus by varying the volume, intensity, and range of motion. According to Nosaka (2008), these components of the eccentric contraction training are the most important for adaptation of the skeletal muscle. We hypothesized that the progressive increase in training load would induce... [to full text]
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Binti, Ahmad Yusof Hazwani. "The Effects of Angiotensin I-Converting Enzyme (ACE) I/D and Alpha-Actinin-3 (ACTN3) R/X Gene Polymorphisms on Human Physical Performance and Health within Malaysian Population." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/14722.

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A disparity population data set in the current literature with limited reports among Asian samples, coupled with the inconsistent findings among different ethnic groups, and lack of information for the involvement of angiotensin I-converting enzyme (ACE) I/D and alpha-actinin-3 (ACTN3) R/X gene polymorphisms in training adaptation have limited the ability of researchers to draw meaningful conclusions pertaining to the effects of these polymorphisms on human physical performance and health. Therefore, this doctoral research implemented three series of studies to examine the effects of ACE I/D and ACTN3 R/X gene polymorphisms on human physical performance and health within the Malaysian population. In the first study, DNA samples were retrieved via buccal cell from 180 Asians from Malaysia (70 males, 110 females) aged 20.4 ± 1.6 years, and 180 Caucasians from Australia (62 males, 118 females) aged 23.3 ± 3.6 years. In the second study, DNA samples were retrieved from 180 well-trained Malaysian athletes (148 males, 32 females) aged 20.5 ± 1.9 years, 180 Malaysian sedentary controls, and 33 intermittent Australian athletes (all males) aged 20.7 ± 4.0 years. Endurance and muscular performances of Malaysian athletes were evaluated with 20 meters Yo-Yo intermittent recovery level 2 and maximal voluntary contraction tests, respectively. In the third study, thirty normotensive, untrained males (ACE genotype: II = 10, ID = 10, and DD = 10), undergone isometric handgrip training (four sets of 2 minutes isometric contractions at 30% of maximal voluntary contraction, with 1 minute resting interval) 3 days per week for 8 weeks. The result from the first study indicated that the distribution of ACE I/D gene polymorphism varied among different ethnic groups, but not to ACTN3 R/X gene polymorphism. The findings obtained from the second study demonstrated that: a) The effects of these polymorphisms on endurance and strength/power performances did not vary by ethnicity, b) The ACE D allele and ACTN3 R allele conferred an advantage in activities that require strength/power, and c) The ACE I allele and ACTN3 X allele did not influence endurance performance. Finding from the final study demonstrated that ACE I/D gene polymorphism had a positive influence in cardiovascular and muscular adaptations following isometric handgrip training among normotensive men. Overall, this research reaffirms the notion that strength/power performance is influenced by the ACE D allele and ACTN3 R allele. In addition, this research concludes that the ACE I/D gene polymorphism modulates response to isometric handgrip training in normotensive men.
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Swaidani, Shadi. "THE ROLE OF ACT1 IN IL-25 DEPENDENT TH2 RESPONSES AND ALLERGIC AIRWAY INFLAMMATION AND AIRWAY HYPERRESPONSIVENESS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1270240862.

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Vilella-Arias, Santiago Andrés. "Estudo de candidatos a biomarcadores moleculares de prognóstico em carcinoma renal de células claras." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/46/46131/tde-20032014-075848/.

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O carcinoma de células renais (CCR) é o tumor mais agressivo que afeta o rim de pessoas adultas. O CCR é uma doença heterogênea, com diferentes alterações moleculares e variados patrões histológicos e clínicos que apresentam evolução diferente. Atualmente apenas variáveis anatomopatológicas clássicas são utilizadas para determinar o prognóstico dos pacientes. Utilizando uma plataforma de microarranjos de DNA, nosso grupo identificou em um trabalho anterior um conjunto de genes que se encontram diferencialmente expressos em tumores de rim. Neste estudo, nove candidatos foram selecionados para avaliação como marcadores de prognóstico no CCR. Foi confirmada a alteração na expressão dos genes ARNTL, ACTN4 e EPAS1 (p < 0,05) em amostras tumorais de CCR através de PCR em tempo real. Adicionalmente, foi observada a alteração da expressão dos genes ARNTL, EPAS1 e CASP7 em linhagens celulares imortalizadas derivadas de tumores renais, recapitulando por tanto, as alterações observadas nos tumores obtidos de pacientes. Posteriormente investigamos o padrão de expressão proteica destes candidatos por imunohistoquímica utilizando microarranjos de tecidos. Foi detectada a diminuição significativa (p < 0,05) da expressão das proteínas ACTN4, ARNTL, CASP7 e EPAS1 em tumores de pacientes com CCR relativamente ao tecido renal não tumoral. Além disso, foi possível determinar valores de imunomarcação capazes de estratificar pacientes com CCR em diferentes grupos de risco quanto à sobrevida câncer-específica, que adicionalmente apresentaram associação significativa com parâmetros anatomopatológicos utilizados na clínica. As imunomarcações de ACTN4, ARNTL, e EPAS1 se mostraram parâmetros independentes de prognóstico de sobrevida dos pacientes. A imunomarcação de CASP7 foi capaz de identificar subgrupos de pacientes com pior prognóstico dentro de um conjunto de pacientes de baixo risco em função do estadio clinico, além de identificar pacientes com menor risco de morte pelo câncer entre aqueles apresentaram recorrência em até 5 após a cirurgia. O conjunto de resultados obtidos aponta para um novo conjunto de biomarcadores moleculares com potencial relevância para auxiliar no prognóstico de pacientes com carcinoma de células renais.
The renal cell carcinoma (RCC) is the most aggressive tumor that affects the kidney in adult people. The RCC is a heterogeneous disease, with many different molecular alterations and varied histological and clinical patterns with different outcome. Currently, only classic anatomopathological variables are used to determine patients\' prognosis. Using a DNA microarray platform, our group identified in a previous work a set of genes differentially expressed in renal tumors. In this study, nine candidates were selected for evaluation as prognostic biomarkers in RCC. Alteration of the gene expression in RCC tumor samples was confirmed for ARNTL, ACTN4 and EPAS1 (p < 0.05) by real time PCR. Additionally, gene expression changes of ARNTL, EPAS1 and CASP7 were also observed in immortalized cell lines derived from renal tumors, recapitulating the expression changes detected in the patients\' tumors. Next, we used tissue microarrays to investigate the protein expression of the selected candidates by immunohistochemistry. Expression of the proteins ACTN4, ARNTL, CASP7 and EPAS1 was detected as significantly downregulated (p < 0.05) in patients´ tumors relative to non-tumor renal tissue. Furthermore, immunostaining patterns of the selected candidates were able to stratify patients with RCC in different risk groups according to cancer-specific survival, which also showed significant associations with anatomopathological parameters used in the clinics. ACTN4, ARNTL and EPAS1 immunostaining resulted as independent prognostic parameters of patient survival. CASP7 immunostaining was able to identify subgroups of patients with worse prognosis in a set of low risk patients as determined by their clinical stage, and also identified patients with lower risk of death from cancer amongst patients that relapsed within 5 years after surgery. Overall, these results point to a new set of molecular biomarkers with potential relevance to help in the prognosis of patients with renal cell carcinoma.
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Velichko, Sharlene, Xu Zhou, Lingxiang Zhu, Johnathon David Anderson, Reen Wu, and Yin Chen. "A Novel Nuclear Function for the Interleukin-17 Signaling Adaptor Protein Act1." PUBLIC LIBRARY SCIENCE, 2016. http://hdl.handle.net/10150/621947.

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In the context of the human airway, interleukin-17A (IL-17A) signaling is associated with severe inflammation, as well as protection against pathogenic infection, particularly at mucosal surfaces such as the airway. The intracellular molecule Act1 has been demonstrated to be an essential mediator of IL-17A signaling. In the cytoplasm, it serves as an adaptor protein, binding to both the intracellular domain of the IL-17 receptor as well as members of the canonical nuclear factor kappa B (NF-kappa B) pathway. It also has enzymatic activity, and serves as an E3 ubiquitin ligase. In the context of airway epithelial cells, we demonstrate for the first time that Act1 is also present in the nucleus, especially after IL-17A stimulation. Ectopic Act1 expression can also increase the nuclear localization of Act1. Act1 can up-regulate the expression and promoter activity of a subset of IL-17A target genes in the absence of IL-17A signaling in a manner that is dependent on its N- and C-terminal domains, but is NF-kappa B independent. Finally, we show that nuclear Act1 can bind to both distal and proximal promoter regions of DEFB4, one of the IL-17A responsive genes. This transcriptional regulatory activity represents a novel function for Act1. Taken together, this is the first report to describe a non-adaptor function of Act1 by directly binding to the promoter region of IL-17A responsive genes and directly regulate their transcription.
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Wagle, John P., Kevin M. Carroll, Aaron J. Cunanan, Alexander Wetmore, Christopher B. Taber, Brad H. DeWeese, Kimitake Sato, Charles A. Stuart, and Michael H. Stone. "Preliminary Investigation Into the Effect of ACTN3 and ACE Polymorphisms on Muscle and Performance Characteristics." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/etsu-works/4663.

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The purpose of this investigation was to explore the phenotypic and performance outcomes associated with ACTN3 and ACE polymorphisms. Ten trained men (age = 25.8 ± 3.0 years, height = 183.3 ± 4.1 cm, body mass = 92.3 ± 9.3 kg, and back squat to body mass ratio = 1.8 ± 0.3) participated. Blood samples were analyzed to determine ACTN3 and ACE polymorphisms. Standing ultrasonography images of the vastus lateralis (VL) were collected to determine whole muscle cross-sectional area (CSA-M), and a percutaneous muscle biopsy of the VL was collected to determine type I–specific CSA (CSA-T1), type II–specific CSA (CSA-T2), and type II to type I CSA ratio (CSA-R). Isometric squats were performed on force platforms with data used to determine peak force (IPF), allometrically scaled peak force (IPFa), and rate of force development (RFD) at various timepoints. One repetition maximum back squats were performed, whereby allometrically scaled dynamic strength (DSa) was determined. Cohen's d effect sizes revealed ACTN3 RR and ACE DD tended to result in greater CSA-M but differ in how they contribute to performance. ACTN3 RR's influence seems to be in the type II fibers, altering maximal strength, and ACE DD may influence RFD capabilities through a favorable CSA-R. Although the findings of the current investigation are limited by the sample size, the findings demonstrate the potential influence of ACTN3 and ACE polymorphisms on isometric and dynamic strength testing. This study may serve as a framework to generate hypotheses regarding the effect of genetics on performance.
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Books on the topic "ACTN1"

1

NA. Math in Actn Intro& Math Actn Alg Graph& MML. Addison Wesley Publishing Company, 2004.

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Allen. Systems in Actn. Not Avail, 1998.

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NA. Expl Offc XP V1 Enhancd& Tec Actn& Actn CD Pk. Addison Wesley Longman, 2005.

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Pearson. Busn in Actn W/Real Upd&videos Busn in Actn. Pearson, 2009.

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NA. Math in Actn : Intro& Math Actn: Alg& 2 Mmls Pk. Addison Wesley Publishing Company, 2005.

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Smorsten. Preface/Actn Sg 2e 068455. Not Avail, 1998.

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Jones, Carol Barton. Eng in Actn: Assignment File. Heinemann Educational Publishers, 1991.

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Pearson. Educ Research&myeducationlab&wetska Actn Pk. Pearson, 2009.

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Pearson. Educational Resrch: Fundmntl&wesska Actn Pk. Pearson, 2009.

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Coulter. Stratg Actn and airlne and Resp. Pearson Education, Limited, 2003.

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Book chapters on the topic "ACTN1"

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Allwood, Jens. "Action theory." In Handbook of Pragmatics, 35–37. Amsterdam: John Benjamins Publishing Company, 2022. http://dx.doi.org/10.1075/hop.m2.act1.

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Biggs, Catherine M., and Stuart E. Turvey. "Chronic Mucocutaneous Candidiasis, ACT1 Deficiency." In Encyclopedia of Medical Immunology, 161–64. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_63.

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Biggs, Catherine M., and Stuart E. Turvey. "Chronic Mucocutaneous Candidiasis, ACT1 Deficiency." In Encyclopedia of Medical Immunology, 1–4. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-9209-2_63-1.

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Macarthur, Daniel G., and Kathryn N. North. "The ACTN3 Gene and Human Performance." In Genetic and Molecular Aspects of Sport Performance, 204–14. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444327335.ch18.

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Jørgensen, Trine N., Natalia V. Giltiay, Angela Johnson, and Xiaoxia Li. "The Role of Act1 in the Control of Autoimmunity." In The Epigenetics of Autoimmune Diseases, 55–74. Chichester, UK: John Wiley & Sons, Ltd, 2009. http://dx.doi.org/10.1002/9780470743553.ch4.

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Wu, Ling, Jarod Zepp, and Xiaoxia Li. "Function of Act1 in IL-17 Family Signaling and Autoimmunity." In Advances in Experimental Medicine and Biology, 223–35. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0106-3_13.

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Gerats, Tom, Jan Zethof, and Michiel Vandenbussche. "Identification and Applications of the Petunia Class II Act1/dTph1 Transposable Element System." In Methods in Molecular Biology, 223–37. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-568-2_16.

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Zhang, Qianying, Jun Ma, Jingyuan Xie, Zhaohui Wang, Bin Zhu, Xu Hao, Li Yang, Hong Ren, and Nan Chen. "Screening of ACTN4 and TRPC6 Mutations in a Chinese Cohort of Patients with Adult-Onset Familial Focal Segmental Glomerulosclerosis." In Contributions to Nephrology, 91–100. Basel: S. KARGER AG, 2013. http://dx.doi.org/10.1159/000348471.

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"ACTN1." In Encyclopedia of Signaling Molecules, 140. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_100106.

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"ACTN2." In Encyclopedia of Signaling Molecules, 140. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_100107.

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Conference papers on the topic "ACTN1"

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Zheng, Yanlei, Yantao Zhou, Guangquan Wang, and Yacheng Liu. "NBI Modeling Realization for SDOTN Based on ACTN." In 2019 IEEE 11th International Conference on Communication Software and Networks (ICCSN). IEEE, 2019. http://dx.doi.org/10.1109/iccsn.2019.8905257.

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Lee, Young, Ricard Vilalta, Ramon Casellas, Ricardo Martinez, and Raul Munoz. "Scalable telemetry and network autonomics in ACTN SDN controller hierarchy." In 2017 19th International Conference on Transparent Optical Networks (ICTON). IEEE, 2017. http://dx.doi.org/10.1109/icton.2017.8025036.

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Jin, Lei, Hessam Tabatabaeehatambakhsh, Chen Chen Jiang, Xu Guang Yan, Jia Yu Wang, Yuan Yuan Zhang, Hamed Yari, et al. "Abstract 4462: ACTN4 stabilises RIPK1 to function as an oncogenic driver in melanoma." 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.am2017-4462.

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Lee, Young, Kaippallimalil John, and Ricard Vilalta. "Extended ACTN Architecture to Enable End-To-End 5G Transport Service Assurance." In 2019 21st International Conference on Transparent Optical Networks (ICTON). IEEE, 2019. http://dx.doi.org/10.1109/icton.2019.8840270.

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Iwakuma, Tomoo. "Abstract LB-303: Metastasis suppression by MDM2 binding protein through inhibition of ACTN4 function." 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-303.

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Qu, Xiaochao, Koop Norbert, Zheng Li, Jing Wang, Zhenxi Zhang, and Gereon Hüttmann. "Multiphoton fluorescence lifetime imaging of Karpas 299 cells using ACT1 antibody conjugated gold nanoparticles." In European Conference on Biomedical Optics. Washington, D.C.: OSA, 2007. http://dx.doi.org/10.1364/ecbo.2007.6630_47.

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Qu, Xiaochao, Koop Norbert, Zheng Li, Jing Wang, Zhenxi Zhang, and Gereon Hüttmann. "Multiphoton fluorescence lifetime imaging of Karpas 299 cells using ACT1 antibody conjugated gold nanoparticles." In European Conference on Biomedical Optics, edited by Tony Wilson and Ammasi Periasamy. SPIE, 2007. http://dx.doi.org/10.1117/12.728239.

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Tan, Yanxia, Yong Zhang, Yanlei Zheng, Yacheng Liu, Yan Shi, Yantao Zhou, Guangquan Wang, and Yuefeng Ji. "Experimental Demonstration of Hierarchical Control over Multi-Vendor SDOTN Networks Based on Extended ACTN." In Asia Communications and Photonics Conference. Washington, D.C.: OSA, 2020. http://dx.doi.org/10.1364/acpc.2020.t3c.5.

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Vilalta, Ricard, Young Lee, Haomian Zhang, Yi Lin, Ramon Casellas, Arturo Mayoral, Ricardo Martínez, Raul Muñoz, Luis Miguel Contreras, and Victor López. "Fully Automated Peer Service Orchestration of Cloud and Network Resources Using ACTN and CSO." In Optical Fiber Communication Conference. Washington, D.C.: OSA, 2017. http://dx.doi.org/10.1364/ofc.2017.tu3l.2.

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Vilalta, Ricard, Ramon Casellas, Ricardo Martinez, Raul Munoz, Young Lee, Haomian Zheng, Yi Lin, Victor Lopez, and Luis Miguel Contreras. "Fully automated peer service orchestration of cloud and network resources using ACTN and CSO." In 2018 International Conference on Optical Network Design and Modeling (ONDM). IEEE, 2018. http://dx.doi.org/10.23919/ondm.2018.8396118.

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Reports on the topic "ACTN1"

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Ceccarelli, D., and Y. Lee, eds. Framework for Abstraction and Control of TE Networks (ACTN). RFC Editor, August 2018. http://dx.doi.org/10.17487/rfc8453.

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Lee, Y., S. Belotti, D. Dhody, D. Ceccarelli, and B. Yoon. Information Model for Abstraction and Control of TE Networks (ACTN). RFC Editor, September 2018. http://dx.doi.org/10.17487/rfc8454.

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Charles Kessel, et al. The Physics Basis For An Advanced Physics And Advanced Technology Tokamak Power Plant Configuration, ARIES-ACT1. Office of Scientific and Technical Information (OSTI), March 2014. http://dx.doi.org/10.2172/1128915.

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Dhody, D., Y. Lee, and D. Ceccarelli. Applicability of the Path Computation Element (PCE) to the Abstraction and Control of TE Networks (ACTN). RFC Editor, July 2019. http://dx.doi.org/10.17487/rfc8637.

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