Academic literature on the topic 'MiR-204'
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Journal articles on the topic "MiR-204"
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Huang, Zhengbiao, and Tianling Deng. "miR-204-3p Regulates Glioma Cell Biological Behaviors via Targeting Protein Kinase B (AKT1)." Journal of Biomaterials and Tissue Engineering 12, no. 12 (December 1, 2022): 2395–400. http://dx.doi.org/10.1166/jbt.2022.3188.
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This study assesses miR-204-3p’s role in glioma. Cells were transfected with miR-204-3pmimics, miR-204-3p inhibitor, or si-AKT1 to measure cell proliferation, invasion, migration and apoptosis. Glioma tissues showed a significantly downregulated miR-204-3p, whose knockdown can significantly promote cell proliferation, migration and invasion. However, all the above changes or cell behavior were inhibited by overexpression of miR-204-3p. miR-204-3p regulated AKT1 and its silence can promote cell proliferation and decrease apoptosis by increasing AKT1 expression. However, si-AKT1 transfection inhibited cell proliferation and promote apoptosis induced by miR-204-3p knockdown. In summary, miR-204-3p regulates glioma cell biological behaviors by targeting AKT1.
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Sun, Xueqin, Shan Su, Guoxiang Zhang, Hong Zhang, and Xiaohui Yu. "MiR-204 suppresses cell proliferation and promotes apoptosis in ovarian granulosa cells via targeting TPT1 in polycystic ovary syndrome." Biochemistry and Cell Biology 97, no. 5 (October 2019): 554–62. http://dx.doi.org/10.1139/bcb-2019-0019.
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MicroRNA (miR)-204 is known to be associated with several different diseases. Polycystic ovary syndrome (PCOS) has the highest incidence rate among the endocrine disorders in females between the ages of 18 and 44. We aimed to illustrate the miR-204 function in PCOS. MiR-204 expression levels in tissue and cell were examined through RT-qPCR. Colony formation assay and MTT assay were applied to detect the cell viability. Flow cytometry was employed to examine the apoptosis and cell cycle in cells. RNA binding protein immunoprecipitation assay and luciferase reporter assay were provided to demonstrate the direct interaction between translationally controlled tumor protein (TPT1) and miR-204. The expression of miR-204 was declined in KGN cells and ovarian cortex tissues of PCOS patients. MiR-204 enhanced the colony formation capacity and cell proliferation in KGN cells. Cell cycle and apoptosis were also influenced by miR-204. Since miR-204 has direct interaction with TPT1, TPT1 overexpression suppressed the miR-204-induced apoptosis and cell cycle alteration in KGN cells. MiR-204 inhibits the cell viability and induces apoptosis and cell cycle arrest by directly interacting with TPT1, indicating a role of miR-204 to be a potential target in the PCOS patients.
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Wang, Zhiguo, Zehui Fang, Runzhang Lu, Hongli Zhao, Tiejun Gong, Dong Liu, Luojia Hong, Jun Ma, and Mei Zhang. "MicroRNA-204 Potentiates the Sensitivity of Acute Myeloid Leukemia Cells to Arsenic Trioxide." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 27, no. 9 (September 23, 2019): 1035–42. http://dx.doi.org/10.3727/096504019x15528367532612.
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Although arsenic trioxide (ATO) is a well-known antileukemic drug used for acute promyelocytic leukemia treatment, the development of ATO resistance is still a big challenge. We previously reported that microRNA-204 (miR-204) was involved in the regulation of acute myeloid leukemia (AML) cell apoptosis, but its role in chemoresistance is poorly understood. In the present study, we showed that miR-204 was significantly increased in AML cells after ATO treatment. Interestingly, the increased miR-204 level that was negatively correlated with ATO induced the decrease in cell viability and baculoviral inhibition of apoptosis protein repeat-containing 6 (BIRC6) expression. Overexpression of miR-204 potentiated ATO-induced AML cell growth inhibition and apoptosis. Furthermore, miR-204 directly targets to the 3′-UTR of BIRC6. Upregulation of miR-204 decreased BIRC6 luciferase activity and expression, which subsequently enhanced the expression of p53. Restoration of BIRC6 markedly reversed the effect of miR-204 on the regulation of AML cell sensitivity to ATO. Taken together, our study demonstrates that miR-204 decreases ATO chemoresistance in AML cells at least partially via promoting BIRC6/p53-mediated apoptosis. miR-204 represents a novel target of ATO, and upregulation of miR-204 may be a useful strategy to improve the efficacy of ATO in AML treatment.
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Du, Youyou, Guanghui Liu, Luosha Zhao, and Rui Yao. "Protective Effect of miR-204 on Doxorubicin-Induced Cardiomyocyte Injury via HMGB1." Oxidative Medicine and Cellular Longevity 2020 (November 19, 2020): 1–16. http://dx.doi.org/10.1155/2020/8819771.
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The toxicity of doxorubicin (DOX) limits its clinical application. Nevertheless, at present, there is no effective drug to prevent DOX-induced cardiac injury. miR-204 is a newly discovered miRNA with many protective effects on cardiovascular diseases. However, little research has been done on the effects of miR-204 on DOX-induced cardiac injury. Our study is aimed at investigating the effect of miR-204 on DOX-induced myocardial injury. An adenoassociated virus system was used to achieve cardiac-specific overexpression of miR-204. Two weeks later, the mice were intraperitoneally injected with DOX (15 mg/kg) to induce cardiac injury. H9c2 myocardial cells were used to validate the role of miR-204 in vitro. Our study showed that miR-204 expression was decreased in DOX-treated hearts. miR-204 overexpression improved cardiac function and alleviated cardiac inflammation, apoptosis, and autophagy induced by DOX. In addition, our results showed that miR-204 prevented DOX-induced injury in cardiomyocytes by directly decreasing HMGB1 expression. Moreover, the overexpression of HMGB1 could offset the protective effects of miR-204 against DOX-induced cardiac injury. In summary, our study showed that miR-204 protected against DOX-induced cardiac injury via the inhibition of HMGB1, and increasing miR-204 expression may be a new treatment option for patients with DOX-induced cardiac injury.
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Song, Rui, Yufeng Zhai, Lihua Ao, David A. Fullerton, and Xianzhong Meng. "MicroRNA-204 Deficiency in Human Aortic Valves Elevates Valvular Osteogenic Activity." International Journal of Molecular Sciences 21, no. 1 (December 20, 2019): 76. http://dx.doi.org/10.3390/ijms21010076.
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Aortic valve interstitial cells (AVICs) play a major role in valvular calcification associated with calcific aortic valve disease (CAVD). Although AVICs from diseased valves display a pro-osteogenic phenotype, the underlying mechanism causing this remains unclear. MicroRNA-204 (miR-204) is a negative regulator of osteoblast differentiation. We sought to analyze miR-204 expression in diseased human aortic valves and determine the role of this miR in AVIC osteogenic activity associated with CAVD pathobiology. In situ hybridization and PCR analysis revealed miR-204 deficiency in diseased valves and in AVICs from diseased valves. MiR-204 mimic suppressed alkaline phosphatase (ALP) expression and calcium deposition in AVICs from diseased valves. MiR-204 antagomir enhanced ALP expression in AVICs from normal valves through induction of Runx2 and Osx, and expression of miR-204 antagomir in mouse aortic valves promoted calcium deposition through up-regulation of Runx2 and Osx. Further, miR-204 mimic suppressed the osteogenic responses to TGF-β1 in AVICs of normal valves. In conclusion, miR-204 deficiency contributes to the mechanism underlying elevated osteogenic activity in diseased aortic valves, and miR-204 is capable of reversing the pro-osteogenic phenotype of AVICs of diseased valves and suppressing AVIC osteogenic response to stimulation. Exogenous miR-204 may have therapeutic potential for inhibiting valvular calcification associated with CAVD progression.
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Su, Qunxue, Hao Shen, Bei Gu, and Ning Zhu. "miR-204-5p Hampers Breast Cancer Malignancy and Affects the Cell Cycle by Targeting PRR11." Computational and Mathematical Methods in Medicine 2022 (January 27, 2022): 1–10. http://dx.doi.org/10.1155/2022/4010947.
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Purpose. To unravel mechanisms of miR-204-5p in breast cancer (BC) cells. Methods. miR-204-5p expression level in BC cell lines was measured by qRT-PCR. Putative binding sites of miR-204-5p on the 3 ′ -untranslated region of PRR11 were predicted by the bioinformatics method and verified by the dual-luciferase method. Protein and mRNA levels of PRR11 in BC were determined by western blot and qRT-PCR. The association between two genes was analyzed by correlation analysis. Cancer cell functions were evaluated through CCK8, flow cytometry, and Transwell approaches. Results. Significant downregulation of miR-204-5p was observed in BC tissue and cells. Cell functional experiments showed the inhibition of miR-204-5p on cell behaviors and cell cycle. PRR11 was the downstream target of miR-204-5p. Inhibition of RPP11 could reverse the impacts of the miR-204-5p inhibitor on cell functions of BC. Conclusion. Our study revealed that the miR-204-5p/PRPP11 axis suppressed BC progression, which may provide a novel insight into the regulatory roles of miR-204-5p.
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Li, Liang-Qing, Dun Pan, Qun Chen, Sheng-Wei Zhang, Di-Ya Xie, Xue-Lan Zheng, and Hui Chen. "Sensitization of Gastric Cancer Cells to 5-FU by MicroRNA-204 Through Targeting the TGFBR2-Mediated Epithelial to Mesenchymal Transition." Cellular Physiology and Biochemistry 47, no. 4 (2018): 1533–45. http://dx.doi.org/10.1159/000490871.
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Background/Aims: Gastric cancer (GC) is the most common gastrointestinal malignancy, causing cancer-related deaths in East Asia. MicroRNAs (miRNAs) are small non-coding RNAs aberrantly expressed in human tumors. In this study, we aim to investigate the roles of miR-204 in the epithelial to mesenchymal transition (EMT)-associated chemosensitivity. Methods: The expression of miR-204 was detected in clinical tumor samples and GC cell lines by real time PCR. Tumor cell’s growth, invasion, and migration were measured by MTT assay, wound healing assay, and transwell invasion assay, respectively. Western blot method was used to detect the protein levels of indicated genes. Luciferase reporter assay was performed to validate the target gene of miR-204. The in vivo role of miR-204 was measured using a xenograft mouse model of GC. Results: By comparing the expressions of miR-204 in human gastric tumors and their adjacent normal tissues, it was disclosed that miR-204 was significantly downregulated in gastric tumors. Moreover, miR-204 was downregulated in multiple GC cell lines compared with normal gastric epithelial cells. Overexpression of miR-204 suppressed GC cells’ proliferation, invasion, and migration. It is noteworthy that 5-FU treatments induced miR-204 expression and suppressed TGF-β pathway. By establishment of 5-FU resistant GC cell line, it was revealed that miR-204 was significantly downregulated in 5-FU resistant GC cells, representing mesenchymal features with downregulation of epithelial marker, while mesenchymal markers were upregulated. We identified TGFBR2 as a direct target of miR-204 by Western blot method and luciferase assay in GC cells and tumor samples as well. In addition, overexpression of miR-204 sensitized GC cells to 5-FU in vitro. Xenograft experiments demonstrated that the combination of miR-204 and 5-FU efficiently inhibited tumor growth and improved survival rate of mice as well. Eventually, we illustrated the restoration of TGFBR2 in miR-204 overexpression GC cells, which recovered resistance to 5-FU treatments compared with miR-204 overexpression GC cells. Conclusion: This study describes a miRNA-based therapeutic strategy against 5-FU resistance in GC, contributing to the development of anti-chemoresistance therapeutic agents.
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Estephan, Leonard E., Michael V. Genuardi, Chad M. Kosanovich, Michael G. Risbano, Yingze Zhang, Nancy Petro, Annie Watson, et al. "Distinct plasma gradients of microRNA-204 in the pulmonary circulation of patients suffering from WHO Groups I and II pulmonary hypertension." Pulmonary Circulation 9, no. 2 (March 28, 2019): 204589401984064. http://dx.doi.org/10.1177/2045894019840646.
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Pulmonary hypertension (PH), a heterogeneous vascular disease, consists of subtypes with overlapping clinical phenotypes. MicroRNAs, small non-coding RNAs that negatively regulate gene expression, have emerged as regulators of PH pathogenesis. The muscle-specific micro RNA (miR)-204 is known to be depleted in diseased pulmonary artery smooth muscle cells (PASMCs), furthering proliferation and promoting PH. Alterations of circulating plasma miR-204 across the trans-pulmonary vascular bed might provide mechanistic insights into the observed intracellular depletion and may help distinguish PH subtypes. MiR-204 levels were quantified at sequential pulmonary vasculature sites in 91 patients with World Health Organization (WHO) Group I pulmonary arterial hypertension (PAH) (n = 47), Group II PH (n = 22), or no PH (n = 22). Blood from the right atrium/superior vena cava, pulmonary artery, and pulmonary capillary wedge was collected. Peripheral blood mononuclear cells (PBMCs) were isolated (n = 5/group). Excretion of miR-204 by PAH-PASMCs was also quantified in vitro. In Group I patients only, miR-204 concentration increased sequentially along the pulmonary vasculature (log fold-change slope = 0.22 [95% CI = 0.06–0.37], P = 0.008). PBMCs revealed insignificant miR-204 variations among PH groups ( P = 0.12). Cultured PAH-PAMSCs displayed a decrease of intracellular miR-204 ( P = 0.0004), and a converse increase of extracellular miR-204 ( P = 0.0018) versus control. The stepwise elevation of circulating miR-204 across the pulmonary vasculature in Group I, but not Group II, PH indicates differences in muscle-specific pathobiology between subtypes. Considering the known importance of miR-204 in PH, these findings may suggest pathologic excretion of miR-204 in Group I PAH by PASMCs, thereby accounting for decreased intracellular miR-204 concentration.
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Qu, Liangliang, Zhongqiu Li, and Pinduan Liu. "mir-204-5p Acts as a Tumor Suppressor by Targeting DNM2 in Osteosarcoma Cells." Journal of Healthcare Engineering 2022 (February 9, 2022): 1–7. http://dx.doi.org/10.1155/2022/8944588.
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Osteosarcoma is a malignant bone tumor composed of interstitial cells. We aim to seek the function of mir-204-5p/DNM2 in osteosarcoma cells. From April 2017 to August 2019, 58 cases of cancer tissues and paracancer tissues were obtained from patients with osteosarcoma in our hospital. qPCR was used to detect mir-204-5p in excisional cancer tissues and paracarcinoma tissues of osteosarcoma patients. The overexpression vector of mir-204-5p was established and transfected into osteosarcoma cells, and the propagation, invasiveness, migration, and apoptosis of osteosarcoma cells were observed. StarBase was employed to forecast the binding site of mir-204-5p and DNM2. The targeting connection of mir-204-5p with DNM2 was detected via double luciferase reporter gene. mir-204-5p was lessened in osteosarcoma ( p < 0.05 ). mir-204-5p overexpression suppressed propagation and accelerated apoptosis of osteosarcoma cells ( p < 0.05 ). The results of double luciferase reporter gene revealed that the fluorescence activity of mir-204-5p was obviously declined when binding to DNM2 ( p < 0.05 ). mir-204-5p functions as a tumor inhibitor by targeting DNM2 in osteosarcoma cells. Our research is helpful to provide new ideas for clinical treatment.
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Cheng, Yuan, Dandan Wang, Feng Wang, Jing Liu, Baorui Huang, Maria Angeles Baker, Jianyong Yin, et al. "Endogenous miR-204 Protects the Kidney against Chronic Injury in Hypertension and Diabetes." Journal of the American Society of Nephrology 31, no. 7 (June 2, 2020): 1539–54. http://dx.doi.org/10.1681/asn.2019101100.
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BackgroundAberrant microRNA (miRNA) expression affects biologic processes and downstream genes that are crucial to CKD initiation or progression. The miRNA miR-204-5p is highly expressed in the kidney but whether miR-204-5p plays any role in the development of chronic renal injury is unknown.MethodsWe used real-time PCR to determine levels of miR-204 in human kidney biopsies and animal models. We generated Mir204 knockout mice and used locked nucleic acid–modified anti-miR to knock down miR-204-5p in mice and rats. We used a number of physiologic, histologic, and molecular techniques to analyze the potential role of miR-204-5p in three models of renal injury.ResultsKidneys of patients with hypertension, hypertensive nephrosclerosis, or diabetic nephropathy exhibited a significant decrease in miR-204-5p compared with controls. Dahl salt-sensitive rats displayed lower levels of renal miR-204-5p compared with partially protected congenic SS.13BN26 rats. Administering anti–miR-204-5p to SS.13BN26 rats exacerbated interlobular artery thickening and renal interstitial fibrosis. In a mouse model of hypertensive renal injury induced by uninephrectomy, angiotensin II, and a high-salt diet, Mir204 gene knockout significantly exacerbated albuminuria, renal interstitial fibrosis, and interlobular artery thickening, despite attenuation of hypertension. In diabetic db/db mice, administering anti–miR-204-5p exacerbated albuminuria and cortical fibrosis without influencing blood glucose levels. In all three models, inhibiting miR-204-5p or deleting Mir204 led to upregulation of protein tyrosine phosphatase SHP2, a target gene of miR-204-5p, and increased phosphorylation of signal transducer and activator of transcription 3, or STAT3, which is an injury-promoting effector of SHP2.ConclusionsThese findings indicate that the highly expressed miR-204-5p plays a prominent role in safeguarding the kidneys against common causes of chronic renal injury.
Dissertations / Theses on the topic "MiR-204"
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Bhat, Rajeshwari Subray. "Study of the role of miR-204 in photoreceptor development." Thesis, Open University, 2016. http://oro.open.ac.uk/48207/.
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MicroRNAs (miRNAs), a class of small non-coding RNAs with a basic role in post-transcriptional regulation of gene expression, are emerging as key players in the control of fundamental biological processes during the differentiation of many tissues and organs. The goal of my thesis is to shed light on the role of specific miRNAs in regulating the retina development especially photoreceptors. In particular, I focused on miR-204, one of the miRNAs our laboratory is mostly focusing on, and whose role in multiple aspects of eye development has been elucidated in the past few years from our lab and other groups. I dissected the role of miR-204 in photoreceptor cell differentiation and maturation by means of in vivo (Oryzias latipes i.e. medaka fish) and in vitro (661W cell line) systems. I found that, the gain-of-function of miR-204 led to an earlier exit of photoreceptor precursors from cell cycle and to a concomitant earlier ‘fate determination’, which in turn resulted in earlier onset of photoreceptor cell formation. Interestingly, I found that the induction of photoreceptor differentiation in 661W cells was accompanied by an upregulation of miR-204 levels, supporting the hypothesis that miR-204 may play a role in cell cycle and/or cell fate determination. To better investigate on this aspect, I demonstrated that Cyclin D1 (Ccnd1) and Cd44 play a key role in miR-204-induced photoreceptor differentiation, as assessed by both in vivo and in vitro experiments. Moreover, I generated two medaka transgenic lines exclusively overexpressing miR-204 either in cone or in rod photoreceptors (TαC:GFP:miR-204 and Rho:TK:GFP:miR-204 respectively). Interestingly, I observed that cones and rods attained their maturation earlier respectively in the TαC:GFP:miR-204 and Rho:TK:GFP:miR-204 lines in comparison with controls. Overall this study strongly suggests a prominent role of miR-204 in photoreceptor differentiation and maturation and sheds further light on the contribution of this miRNA to ocular development and function.
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Migliore, Chiara Maria. "RNA-sequencing based identification of microRNA-204 targets." Doctoral thesis, Università degli studi di Trieste, 2011. http://hdl.handle.net/10077/4595.
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2009/2010With the completion of the sequencing and annotation of hundreds of genomes, and the accumulation of data on the mammalian transcriptome, greater emphasis has been placed on elucidating the function of non-coding DNA and RNA sequences. It is well known that the non-coding portion of the genome can transcribe functional RNAs. Several categories of non-coding RNAs (ncRNAs) have been defined, such as transport RNAs (tRNAs) ribosomal RNAs (rRNAs), small nuclear RNAs (snRNAs) and small nucleolar RNAs (snoRNAs). A larger group of ncRNAs comprises the so-called microRNAs (miRNAs) and long non-coding RNAs serving key regulatory roles. It has been shown that miRNAs directly target a large number of genes, thus affecting significantly major pathways. In my project, I focused on miR-204, a microRNA that is highly conserved from zebrafish to human and located in the sixth intron of the human TRPM3 gene. I sought to identify mir-204 targets by using the Medaka fish (Oryzias latipes), where mir-204 is expressed at very low levels in the nervous system, as a model for perturbation of the mir-204 network. Transient transgenic Medaka fish were produced to knock down and over-express mir-204. Next-generation sequencing was used to sequence the Medaka transcriptome, dissect the putative targets of miR-204, and thus gain further insight about its function. Potential target genes of mir-204 were selected by choosing genes, which presented lower expression in the wild-type (wt) fish than in the knock down, a lower expression in the over-expression than in the wt and, finally, a higher expression in the knock down than in the over-expression. At the same time, I collected a list of putative miR-204 mouse and human targets using the prediction softwares miRanda, PicTar and TargetScan, obtained the Medaka orthologues and verified that the selected genes in Medaka had a statistically significant enrichment in miR-204 targets as compared to the complete set of genes obtained from the RNA-Sequencing approach. The combined RNA-Sequencing and bioinformatics analysis revealed 147 predicted targets of mir-204, which showed a significant enrichment for the axon guidance pathway. In order to confirm this data, real time quantitative PCR has been performed on total RNA from wt and morphant fish. Results showed a higher expression in the knock down fish for 15 out of 25 putative targets (Neo1, Trim71, Ddx3y, Prkar1a, MyoX, Sema3B, Sema3F, Ptprg, Slit2, Epha4, Epha7, Amot, Lpp, Odz4, Jarid2). I further validated these genes by both Q-PCR and luciferase assays. To this aim, I cloned five putative target sequences into the 3’UTR of a luciferase reporter vector (pGL3-TK-luc Promega) to use them in luciferase assays: co-transfection with miR-204 reduced the luciferase activity of Sema3F, belonging to the class of receptors involved upstream of the axon guidance pathway. These results indicate that mir-204 directly targets key genes involved in the axon guidance pathway such as Sema3F in the nervous system. Further validation of the disruption of axon guidance in the transgenic fish has been undertaken in vivo by our collaborators: the experiment demonstrated a clear role of this microRNA in axon path finding during retinal development.
XXII Ciclo
1981
Books on the topic "MiR-204"
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Music, Alfred. Cantata No. 204 -- Ich Bin in Mir Vergnugt: Soprano Solo. Alfred Publishing Company, Incorporated, 1985.
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Bach, Johann Sebastian. Cantatas Nos. 204, Ich bin in mir vergnught (G) and 205 Zerreisset, Zersprenget: Miniature Score, Kalmus Edition. Alfred Publishing Company, 1985.
Find full textBook chapters on the topic "MiR-204"
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"Abkürzungen." In Das Geschlecht in mir, edited by Gerhard Schreiber, XXIII—XXIV. Berlin, Boston: De Gruyter, 2019. http://dx.doi.org/10.1515/9783110614626-204.
Full textConference papers on the topic "MiR-204"
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Ryan, Jacqueline M., Amanda Tivnan, Isabella Bray, Joanna Fay, Andrew M. Davidoff, Lorraine Tracey, and Raymond Stallings. "Abstract 130: MiR-204 acts as a tumor suppressor in neuroblastoma through down-regulation of the neurotrophic receptor TrkB." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-130.
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Koga, T., K. Migita, M. Umeda, F. Nonaka, S.-Y. Kawashiri, N. Iwamoto, K. Ichinose, et al. "FRI0620 MIR-204-3P inhibits the production of TLR4-related cytokines in familial mediterranean fever by targeting the PIK3 signaling pathway." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.2813.
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