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Статті в журналах з теми "DEPDC1A"
Kassambara, Alboukadel, Matthieu Schoenhals, Jérôme Moreaux, Jean-Luc Veyrune, Thierry Rème, Hartmut Goldschmidt, Dirk Hose, and Bernard Klein. "Inhibition of DEPDC1A, a Bad Prognostic Marker in Multiple Myeloma, Delays Growth and Induces Mature Plasma Cell Markers in Malignant Plasma Cells." PLoS ONE 8, no. 4 (April 30, 2013): e62752. http://dx.doi.org/10.1371/journal.pone.0062752.
Повний текст джерелаXu, Wei, Juan Wang, Jinfu Xu, Shenyi Li, Ranran Zhang, Cong Shen, Min Xie, Bo Zheng, and Menghui Gu. "Long non-coding RNA DEPDC1-AS1 promotes proliferation and migration of human gastric cancer cells HGC-27 via the human antigen R–F11R pathway." Journal of International Medical Research 50, no. 4 (April 2022): 030006052210931. http://dx.doi.org/10.1177/03000605221093135.
Повний текст джерелаXu, Wei, Juan Wang, Jinfu Xu, Shenyi Li, Ranran Zhang, Cong Shen, Min Xie, Bo Zheng, and Menghui Gu. "Long non-coding RNA DEPDC1-AS1 promotes proliferation and migration of human gastric cancer cells HGC-27 via the human antigen R–F11R pathway." Journal of International Medical Research 50, no. 4 (April 2022): 030006052210931. http://dx.doi.org/10.1177/03000605221093135.
Повний текст джерелаHu, Feng, Ki On Fong, May P. L. Cheung, Jessica A. J. Liu, Rui Liang, Tsz Wai Li, Rakesh Sharma, Philip P. C. Ip, Xintao Yang, and Martin Cheung. "Abstract 5971: DEPDC1B promotes melanoma angiogenesis and metastasis through sequestration of ubiquitin ligase CDC16 to stabilize secreted SCUBE3." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5971. http://dx.doi.org/10.1158/1538-7445.am2022-5971.
Повний текст джерелаAhuja, Palak, and Kailash Singh. "In Silico Approach for SAR Analysis of the Predicted Model of DEPDC1B: A Novel Target for Oral Cancer." Advances in Bioinformatics 2016 (February 29, 2016): 1–8. http://dx.doi.org/10.1155/2016/3136024.
Повний текст джерелаLou, Tingting, Luqing Zhang, Zongshan Jin, Chundi Miao, Jinqiu Wang, and Kongliang Ke. "miR-455-5p enhances 5-fluorouracil sensitivity in colorectal cancer cells by targeting PIK3R1 and DEPDC1." Open Medicine 17, no. 1 (January 1, 2022): 847–56. http://dx.doi.org/10.1515/med-2022-0474.
Повний текст джерелаHuang, Guangzhao, Su Chen, Jumpei Washio, Grace Paka Paka Lubamba, Nobuhiro Takahashi та Chunjie Li. "Glycolysis-Related Gene Analyses Indicate That DEPDC1 Promotes the Malignant Progression of Oral Squamous Cell Carcinoma via the WNT/β-Catenin Signaling Pathway". International Journal of Molecular Sciences 24, № 3 (19 січня 2023): 1992. http://dx.doi.org/10.3390/ijms24031992.
Повний текст джерелаBin, Xiaoyun, Zongjiang Luo, Jianchu Wang, and Sufang Zhou. "Identification of a Five Immune Term Signature for Prognosis and Therapy Options (Immunotherapy versus Targeted Therapy) for Patients with Hepatocellular Carcinoma." Computational and Mathematical Methods in Medicine 2023 (February 2, 2023): 1–17. http://dx.doi.org/10.1155/2023/8958962.
Повний текст джерелаPang, Yuzhi, Feifei Xie, Hui Cao, Chunmeng Wang, Meijun Zhu, Xiaoxiao Liu, Xiaojing Lu, et al. "Mutational inactivation of mTORC1 repressor gene DEPDC5 in human gastrointestinal stromal tumors." Proceedings of the National Academy of Sciences 116, no. 45 (October 21, 2019): 22746–53. http://dx.doi.org/10.1073/pnas.1914542116.
Повний текст джерелаMotomura, Takashi, Yuki Ono, Ken Shirabe, Takasuke Fukuhara, Hideyuki Konishi, Yohei Mano, Takeo Toshima, et al. "Neither MICA Nor DEPDC5 Genetic Polymorphisms Correlate with Hepatocellular Carcinoma Recurrence following Hepatectomy." HPB Surgery 2012 (October 24, 2012): 1–6. http://dx.doi.org/10.1155/2012/185496.
Повний текст джерелаДисертації з теми "DEPDC1A"
Marotta, Carolina. "The role of DEPDC1 (DEP domain containing 1) in breast cancer aggressiveness." Doctoral thesis, Università degli studi di Trieste, 2013. http://hdl.handle.net/10077/8641.
Повний текст джерелаMetastasis formation is the final step in a solid tumour progression and is the most common cause of death in cancer patients. Therefore novel therapeutic strategies to prevent development of metastases have a potential impact on cancer mortality. In the last years, work from our lab has identified that, following oncogenic signalling, the phosphorylation-dependent prolyl-isomerase Pin1 amplifies mutant p53 oncogenic functions. In particular, we have demonstrated the relevance of a Pin1/mutant p53 axis in controlling directly a transcriptional “ten genes signature” program relevant for tumour growth and invasion. This signature includes genes relevant for breast cancer progression, correlated to poor outcome of breast cancer patients. Among these, we have unveiled DEPDC1 as a potent promoter of invasiveness and migration in MDA MB231 triple negative breast cancer (TNBC) cells. This gene is has been found overexpressed in different mouse and human tumours, such as breast carcinoma, colorectal and lung adenocarcinomas. The aim of my PhD work was to investigate the role of DEPDC1 in the cancer progression that is linked to cell-biological traits associated with high-grade malignancy - including motility, invasiveness and loss of polarity. We found that the high DEPDC1 expression level positively correlates with clinical outcome and aggressiveness in breast cancer and we demonstrate that DEPDC1 regulates important phenotypes involved in tumour formation and progression. First, we identified a role of DEPDC1 in promoting aggressive cancer phenotypes in vitro by regulating cell motility, polarity and proliferation. Second, we have evaluated that the establishment of lung metastasis in vivo in mice was reduced upon inhibition of DEPDC1. Third, we demonstrate the tumorigenic potential of DEPDC1-V1 alone or cooperating with oncogenic H-Ras on induction of malignant cell transformation. Finally, a preliminary data shows that DEPDC1 is also able to increase the efficiency of mammosphere formation of breast cancer cells, implicating a role in cancer stemness. Until now, our results support the strong impact of DEPDC1 on tumour progression while molecular pathways perturbed by DEPDC1 and by which drive the cancer progression are still unknown. However, our analysis of RNA-seq data upon silencing of DEPDC1, suggests the mechanism by which DEPDC1 could induce an aggressive phenotype altering the gene expression profile of breast cancer cells. Future studies will address the molecular networks by which DEPDC1 drives the metastatic cancer progression that could be useful for discovering the novel therapeutic targets and diagnostic markers in breast cancer.
XXIV Ciclo
1983
Tosi, Anna. "Identification of a HLA-A*0201-restricted immunogenic epitope from the universal tumor antigen DEPDC1." Doctoral thesis, Università degli studi di Padova, 2017. http://hdl.handle.net/11577/3424867.
Повний текст джерелаL’identificazione di antigeni tumore-specifici universali condivisi tra più pazienti e/o tra più tumori diversi, è di grande importanza per superare le limitazioni pratiche dell’immunoterapia oncologica personalizzata. Il coinvolgimento di DEPDC1 in molti aspetti del processo tumorale, come, ad esempio, nella proliferazione cellulare, nell’anti-apoptosi e nell’invasione cellulare, è stato supportato da lavori pubblicati di recente, suggerendo che tale proteina possa svolgere ruoli chiave nel processo oncogeno. In questo studio riportiamo che l’espressione di DEPDC1 è sovra-regolata in molti tipi di tumori umani, e strettamente collegata ad una prognosi avversa; per questo motivo DEPDC1 può essere considerato come un nuovo antigene tumorale universale potenzialmente adatto per il targeting di molti tumori diversi. A questo proposito, riportiamo l’identificazione di un epitopo immunogenico derivato da DEPDC1 ristretto per la molecola HLA-A*0201, capace di indurre linfociti T citotossici (CTL) esercitanti una forte e specifica risposta funzionale in vitro, in risposta non solo a cellule caricate con il peptide ma anche in risposta a cellule di tumore al seno triplo negativo (TNBC) che esprimono in modo endogeno la proteina DEPDC1. Tali CTL sono anche attivi in modo terapeutico in vivo, in seguito al loro trasferimento adottivo in topi immunodeficienti, nei confronti di xenotrapianti di cellule di TNBC umane. Complessivamente, questi dati forniscono evidenze a supporto dell’uso di questo epitopo antigenico derivante da DEPDC1 come un nuovo strumento per lo sviluppo di strategie immunoterapeutiche per pazienti HLA-A*0201 con TNBC, e potenzialmente con molti altri tipi di tumore. Inoltre, poiché ulteriori miglioramenti negli approcci di immunoterapia necessitano di una comprensione dettagliata delle dinamiche cellulari all’interno del microambiente tumorale, programmiamo di usare un approccio di multiplexing digital pathology per studiare le strette relazioni che i linfociti adottivamente trasferiti possono stabilire con le cellule di TNBC in topi portanti il tumore. I benefici dell’immunoistochimica multispettrale, combinati con lo sviluppo di software per la quantificazione, stanno rendendo questa metodologia un strumento sempre più potente nell’analisi a nella caratterizzazione di processi tessutali e cellulari, supportando il potenziale diagnostico con lo scopo di migliorare le terapie.
MARCHESI, STEFANO. "DEPDC-1B MODULATES RHOA-DEPENDENT CELL ADHESION DURING MITOTIC ENTRY." Doctoral thesis, Università degli Studi di Milano, 2011. http://hdl.handle.net/2434/214609.
Повний текст джерелаDE, FUSCO ANTONIO. "The role of DEPDC5 in the pathogenesis of mTOR-dependent epilepsy and focal cortical dysplasia." Doctoral thesis, Università degli studi di Genova, 2020. http://hdl.handle.net/11567/993832.
Повний текст джерелаCERULLO, MARIA SABINA. "Investigating the effect of Depdc5 cKO: insights on synaptic transmission, plasticity and its role in mTOR-related epilepsy." Doctoral thesis, Università degli studi di Genova, 2021. http://hdl.handle.net/11567/1045171.
Повний текст джерелаMotta, B. M. "UNA VARIANTE ALLELICA NEL LOCUS DEL GENE DEP DOMAIN CONTAINING 5 (DEPDC5) SI ASSOCIA AD AVANZATA FIBROSI IN SOGGETTI CON INFEZIONE CRONICA DA HCV." Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/233993.
Повний текст джерелаBackground and aims Two recent genome-wide association studies (GWAS) performed in Japanese populations showed that the DEP domain containing 5 (DEPDC5) and the MHC class I polypeptide-related sequence A (MICA) locus are associated with susceptibility to hepatocellular carcinoma (HCC) in individuals with chronic hepatitis C (HCV) infection. The effect of these variants has not been assessed in Europeans. The aim of the study was to investigate the effect of DEPDC rs1012068, and MICA rs2596542 on the HCC risk and liver fibrosis in Europeans. Methods The genetic variants were genotyped in an Italian cohort of HCV positive individuals with (n=149) and without HCC (n=328). The significant associations were validated in an independent European cohort from Leipzig (n=323). Results Neither the DEPDC5 or MICA variants associate with HCC in the Italian cohort. An increased risk of developing severe fibrosis was observed for each DEPDC5 G allele in the Italian cohort (Odds Ratio (OR)=1.46; 95% confidence interval(C:I.) 1.04-2.04; p-value=0.027). No association between MICA rs2596542 and severe fibrosis was observed. Consistently an increased risk of severe fibrosis was observed for each DEPDC5 G allele in the Leipzig cohort (OR=1.57; 95% C:I. 1.14-2.16; p-value=0.006). Conclusions DEPDC5 and MICA are not associated with the risk of HCV-related HCC onset in Europeans. However, a higher risk of developing severe fibrosis is associated with the DEPDC5 rs1012068 variant in Europeans with chronic HCV infection.
Calbiac, Hortense de. "Mechanisms of C9ORF72 pathogenicity and related autophagy impairment in amyotrophic lateral sclerosis Sqstm1 knockdown causes a locomotor phenotype ameliorated by rapamycin in a zebrafish model of ALS/FTLD Depdc5 knockdown causes mTOR-dependent motor hyperactivity in zebrafish." Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS561.
Повний текст джерелаTo investigate the pathogenic mechanisms induced by SQSTM1 mutations in ALS, we developed a zebrafish model of sqstm1 haploinsufficiency. We observed that loss of function of sqstm1 leads to a specific motor phenotype. To elucidate the common cellular mechanisms underlying motor neuron degeneration in ALS, we analyzedc9orf72 and sqstm1 epistatic interactions inzebrafish. C9orf72 and sqstm1 partial inhibitions have an additive effect and C9ORF72 rescues the phenotype induced by sqstm1 knockdown. Thus, both proteins belong to the same pathway and c9orf72 acts downstream of sqstm1. Also, we observed that depletion of these genes in mouse motor neurons primary cultures leads to the early death of motor neurons associated with autophagy impairment. To develop a vertebrate model that recapitulates the different mechanisms associated withthe C9ORF72 HRE pathogenicity in ALS, we combined the partial inhibition of c9orf72 with the expression of the DPRs in zebrafish. This induces a robust motor phenotype characterized by locomotor defects and paralysis. Focusing on GP repeats, we observed that the loss of function of c9orf72 is essential to inhibitpoly(GP) clearance.This is associated with SQSTM1/p62 accumulation, severe motor neurons abnormalities and loss. These phenotypes are rescued by the inhibition of caspase 9, a regulator of apoptosis. Also, rapamycinis able to improve the clearance of poly(GP) and p62, with restored swim and motor neurons features, thus confirming the role of C9ORF72 in autophagy.These results show that DPR toxicity is related to lowered expression of C9ORF72, suggesting that both gain and loss of function synergize in the C9ORF72 HRE pathogenicity
Chen, Kuan-Hsuan, and 陳冠璇. "Generation and Characterization of MonoclonalAntibodies Against NPC2 And DEPDC6 Protein." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/vw8dq5.
Повний текст джерела國立陽明大學
公共衛生研究所
97
Glycine N-methylatransferase gene (GNMT) is a tumor suppressor gene, its’ expression was found to be down-regulated in HCC. By using a yeast-two hybrid system, we have recently identified that GNMT could interact with DEP domain containing 6 (DEPDC6) and Neimann-Pick disease type C2 (NPC2) proteins. The goals of this study are: (1) to generate monoclonal and polyclonal NPC2 and DEPDC6 antibodies; (2) to study the expression of NPC2 and DEPDC6 in multiple mouse organs, different cell lines and human cancer tissue arrays; (3) to investigate the expression of NPC2 and DEPDC6 in MCD (Methionine-Coline dificient)-diet induced mouse fatty liver model. Polyclonal and monoclonal antibodies against NPC2 and DEPDC6 were generated by injecting recombinant proteins into animals. The epitopes of monoclonal antibodies will be determined by phage display assay. Results from western blot analysis demonstrated that NPC2 protein is mainly expressed in the epididymis, kidney, lung, testis, utures, large and small intestines of WT mice. DEPDC6 is expressed in the spleen, liver, testis, pancrea, epididymis and large intesine of WT mice. In vitro, endogenous NPC2 could be detected in Hela, LNCaP, HepG2 and SK-Hep1 cells. On the other hand, endogenous DEPDC6 were found to express in BT-20, HS578T, NS-1, Hela, LNCaP, SK-Hep1,HepG2, Hep3B, HuH6, HuH7, HA22T and HA59T cells. We further used multiple human cancer tissue arrays to detect the expression of NPC2 and DEPDC6. The data showed that DEPDC6 expressed in the normal stomach,ovary,esophagus and cervix tissues. It is worthy to note that DEPDC6 was up-regulated in breast cancer, pancreas cancer, kidney cancer, colon cancer and rectum cancer using immunohistochemistry staining. To mimic human fatty liver formation, WT and Gnmt-/- mice were fed a MCD-diet to induce hepatic steatohepatitis, and changes in expression levels of NPC2 and DEPDC6 were detected using western blot analysis. The expression of di-glycosylated form of NPC2 was enhanced and that of the mono-glycosylated form of NPC2 was significantly reduced in MCD-fed female WT and Gnmt-/- mice. In contrast, the expression of DEPDC6 was no significant changes in Gnmt-/- mice as compared to WT littermates. Therefore, our NPC2 and DEPDC6 antibodies will be useful to explore the functional roles of GNMT, NPC2, and DEPDC6 in liver disease.
Li, Chung-Hsien, and 李忠憲. "A Study of the Interactions among GNMT, DEPDC6 and P-Rex2." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/84000966323155174750.
Повний текст джерела國立陽明大學
公共衛生研究所
98
Glycine N-methyltransferase (GNMT) is abundant in liver. It affects cellular methylation potential and DNA stability by regulating the ratio of S-adenosylmethionine to S-adenosylhomocysteine and serving as the major folate binding protein in the liver. The expression of GNMT is down-regulated in human hepatocellular carcinoma (HCC). In addition, GNMT knockout mice developed HCC spontaneously. Therefore, GNMT is a tumor suppressor gene for liver cancer. However, it has been reported that sarcosine, a metabolic product of GNMT enzymatic activity, can serve as a biomarker of prostate cancer progression and metastasis. In order to study the role of GNMT in carcinogenesis, we used yeast two hybrid screen to identify a GNMT interacting protein, DEP domain containing 6 (DEPDC6). It has been reported that DEPDC6 is an mTOR binding protein that normally functions to inhibit the mTOR activity. Results from a phylogenetic analysis indicate that the first DEP domain of DEPDC6 clustered with P-Rex2, a regulator of the small guanosine triphosphatase Rac, linking mTOR signaling to Rac activation and cell migration. P-REX2 has been identified as a direct regulator of PTEN activity and as a potential oncoprotein. In this study, we study the interactions among GNMT, DEPDC6 and P-Rex2. Results from reciprocal co-immunoprecipitation assays demonstrated that P-Rex2, GNMT, DEPDC6 and mTOR could interact with each other. In addition, the DH-PH, PDZ and InsPx4-Phosphatase domains of P-Rex2 were involved in the interactions with GNMT and DEPDC6. Moreover, the PDZ domain of DEPDC6 mediated the interaction with P-Rex2. Results from gel filtration assay demonstrated cofractionation of P-Rex2, GNMT, DEPDC6 and mTOR in 293T cell extracts. Together, these indicated that P-Rex2, GNMT, DEPDC6 and mTOR could present in the same complex. In regard to the functional roles of these interactions, we demonstrated that GNMT could disrupt the interaction between mTOR and DEPDC6. In addition, overexpression of P-Rex2 could positively regulate the expression of DEPDC6. Moreover, overexpression of GNMT and DEPDC6 had no effects on the cell cycle progression of 293T cells. Finally, results from Rac-GEF assay indicated that DEPDC6 could interact with activated Rac and activate the Rac slightly.
Wilson, Jasmine Joy. "DEPDC5 is a metabolic checkpoint regulator in the B cell AA-mTORC1 pathway." Thesis, 2020. http://hdl.handle.net/2440/128586.
Повний текст джерелаThesis (Ph.D.) -- University of Adelaide, School of Biological Sciences, 2020
Книги з теми "DEPDC1A"
Tantiwiramanond, Darunee. Development and Education Program for Daughters and Communities Center (DEPDC). Bangkok, Thailand: Women's Action and Resource Initiative, 1996.
Знайти повний текст джерелаЧастини книг з теми "DEPDC1A"
Lukas, Thomas J., Daniela V. Rosa, Luiz Alexandre V. Magno, Bruno R. Souza, Marco A. Romano-Silva, Hisao Masai, Kazuhisa Kohda, et al. "Depdc2." In Encyclopedia of Signaling Molecules, 518. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100346.
Повний текст джерела"Depdc2." In Encyclopedia of Signaling Molecules, 1352. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_100971.
Повний текст джерелаТези доповідей конференцій з теми "DEPDC1A"
Lazarin Torrezan, Giovana, Laura Cristina Burato Da Veiga, Andrea Maria Abud Priedols, Ana Luiza Decanini Miranda de Souza, and Mauro Audi. "SÍNDROME DO GENE DEPDC5 E A REALIDADE VIRTUAL." In VII NEUROCOR. ,: Even3, 2023. http://dx.doi.org/10.29327/viineurocor.553286.
Повний текст джерелаPadi, Sathish K. R., Neha Singh, Ghassan Mouneimne, Andrew S. Kraft, and Koichi Okumura. "Abstract PR01: Phosphorylation of DEPDC5 by the Pim-1 protein kinase, a cancer driver, stimulates mTORC1 activity by regulating the DEPDC5- Rag GTPase interaction." In Abstracts: AACR Special Conference on Targeting PI3K/mTOR Signaling; November 30-December 8, 2018; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.pi3k-mtor18-pr01.
Повний текст джерелаSharma, A., K. Konstantinos, A. Jayaraman, A. Mann, S. J. Robertson, S. M. Best, and M. Bosmann. "DEPDC7 Augments Anti-Viral Immune Response Through Regulation of Cytokine Release in Macrophages and During Lung Injury." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2185.
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