Academic literature on the topic 'DEPDC1A'
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Journal articles on the topic "DEPDC1A"
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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.
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Xu, 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.
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Objective Long non-coding (lnc) RNAs are critical regulators in carcinogenesis. The novel lncRNA DEPDC1 antisense RNA 1 ( DEPDC1-AS1) was recently associated with poor prognosis in triple-negative breast cancer and lung adenocarcinoma. However, its role in regulating the malignant progression of gastric cancer (GC) and its molecular mechanism are unclear. We herein explored the functions of DEPDC1-AS1 in GC progression. Methods DEPDC1-AS1 expression and prognosis in GC tissues were examined by bioinformatics analysis and quantitative reverse transcription polymerase chain reaction. The DEPDC1-AS1 function in GC cells was explored by the cell counting kit-8 assay, colony formation assay, Transwell assay, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, 5-ethynyl-2′-deoxyuridine-incorporation, and the xenograft tumor model. The DEPDC1-AS1 and human antigen (Hu)R interaction was determined by RNA pull-down and RNA immunoprecipitation. Results DEPDC1-AS1 was overexpressed in GC tissues and cell lines, and associated with a worse prognosis in GC patients. In vitro and in vivo assays showed that DEPDC1-AS1 promoted HGC-27 cell proliferation and migration. Mechanistically, DEPDC1-AS1 served as a scaffold by combining with HuR to target the specific mRNA F11R. Conclusion DEPDC1-AS1 plays a crucial role in GC development and progression and is a potential biomarker for the early detection or prognosis of GC.
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Xu, 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.
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Objective Long non-coding (lnc) RNAs are critical regulators in carcinogenesis. The novel lncRNA DEPDC1 antisense RNA 1 ( DEPDC1-AS1) was recently associated with poor prognosis in triple-negative breast cancer and lung adenocarcinoma. However, its role in regulating the malignant progression of gastric cancer (GC) and its molecular mechanism are unclear. We herein explored the functions of DEPDC1-AS1 in GC progression. Methods DEPDC1-AS1 expression and prognosis in GC tissues were examined by bioinformatics analysis and quantitative reverse transcription polymerase chain reaction. The DEPDC1-AS1 function in GC cells was explored by the cell counting kit-8 assay, colony formation assay, Transwell assay, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, 5-ethynyl-2′-deoxyuridine-incorporation, and the xenograft tumor model. The DEPDC1-AS1 and human antigen (Hu)R interaction was determined by RNA pull-down and RNA immunoprecipitation. Results DEPDC1-AS1 was overexpressed in GC tissues and cell lines, and associated with a worse prognosis in GC patients. In vitro and in vivo assays showed that DEPDC1-AS1 promoted HGC-27 cell proliferation and migration. Mechanistically, DEPDC1-AS1 served as a scaffold by combining with HuR to target the specific mRNA F11R. Conclusion DEPDC1-AS1 plays a crucial role in GC development and progression and is a potential biomarker for the early detection or prognosis of GC.
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Hu, 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.
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Abstract The ability of melanoma to acquire metastasis through the induction of angiogenesis is one of the major causes of skin cancer death. Here, we find that high transcript levels of DEPDC1B in cutaneous melanomas are significantly associated with a poor prognosis. Tissue microarray analysis indicates DEPDC1B expression is positively correlated with SOX10 in the different stages of melanoma. Consistently, DEPDC1B is both required and sufficient for melanoma growth, metastasis, angiogenesis, and functions as a direct downstream target of SOX10 to partly mediate its oncogenic activity. In contrast to other tumor types, the DEPDC1B-mediated enhancement of melanoma metastatic potential is not dependent on the activities of RHO GTPase signaling and canonical Wnt signaling, but is acquired through secretion of SCUBE3, which is crucial for promoting angiogenesis in vitro and in vivo. Mechanistically, DEPDC1B regulates SCUBE3 protein stability through the competitive association with ubiquitin ligase CDC16 to prevent SCUBE3 from undergoing degradation via the ubiquitin-proteasome pathway. Importantly, expression of SOX10, DEPDC1B, and SCUBE3 are positively correlated with microvessel density in the advanced stage of melanomas. In conclusion, we reveal a SOX10-DEPDC1B-SCUBE3 regulatory axis promotes melanoma angiogenesis and metastasis, which suggests targeting secreted SCUBE3 can be a therapeutic strategy against metastatic melanoma. Citation Format: Feng Hu, Ki On Fong, May P.L Cheung, Jessica A.J Liu, Rui Liang, Tsz Wai Li, Rakesh Sharma, Philip P.C Ip, Xintao Yang, Martin Cheung. DEPDC1B promotes melanoma angiogenesis and metastasis through sequestration of ubiquitin ligase CDC16 to stabilize secreted SCUBE3 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5971.
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Ahuja, 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.
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With the incidence rate of oral carcinogenesis increasing in the Southeast-Asian countries, due to increase in the consumption of tobacco and betel quid as well as infection from human papillomavirus, specifically type 16, it becomes crucial to predict the transition of premalignant lesion to cancerous tissue at an initial stage in order to control the process of oncogenesis. DEPDC1B, downregulated in the presence of E2 protein, was recently found to be overexpressed in oral cancer, which can possibly be explained by the disruption of the E2 open reading frame upon the integration of viral genome into the host genome. DEPDC1B mediates its effect by directly interacting with Rac1 protein, which is known to regulate important cell signaling pathways. Therefore, DEPDC1B can be a potential biomarker as well as a therapeutic target for diagnosing and curing the disease. However, the lack of 3D model of the structure makes the utilization of DEPDC1B as a therapeutic target difficult. The present study focuses on the prediction of a suitable 3D model of the protein as well as the analysis of protein-protein interaction between DEPDC1B and Rac1 protein using PatchDock web server along with the identification of allosteric or regulatory sites of DEPDC1B.
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Lou, 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.
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Abstract Our previous study has demonstrated that miR-455-5p was a tumor suppressor in colorectal cancer (CRC). This study aimed to investigate the role of miR-455-5p in 5-fluorouracil (5-Fu) in CRC. The expression of miR-455-5p, PIK3R1, and DEPDC1 was analyzed in HT-29 cells after treatment with different concentrations (0, 0.5, 2.5, and 12.5 μM) of 5-Fu. The effects of miR-455-5p on cell proliferation and apoptosis were analyzed by CCK-8 and flow cytometry. PIK3R1 and DEPDC1 were overexpressed to measure the mechanism of miR-455-5p on 5-Fu sensitivity. And the direct binding between miR-455-5p and DEPDC1 was detected by a dual-luciferase reporter assay. We found that miR-455-5p decreased, while PIK3R1 and DEPDC1 increased after 5-Fu treatment. miR-455-5p mimic significantly suppressed cell viability and elevated cell apoptosis in 5-Fu-treated HT-29 cells, whereas miR-455-5p inhibitor showed the opposite effects. Overexpression of PIK3R1 and DEPDC1 could attenuate the effects of miR-455-5p mimic on the viability and apoptosis of 5-Fu-treated cells. miR-455-5p could directly bind to DEPDC1 in HT-29 cells. In conclusion, miR-455-5p enhanced 5-Fu sensitivity by targeting PIK3R1 and DEPDC1 in CRC. This study provides a novel role of miR-455-5p in CRC and restoring miR-455-5p might be a therapeutic strategy to enhance chemosensitivity to 5-Fu.
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Huang, Guangzhao, Su Chen, Jumpei Washio, Grace Paka Paka Lubamba, Nobuhiro Takahashi, and 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, no. 3 (January 19, 2023): 1992. http://dx.doi.org/10.3390/ijms24031992.
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Increasing evidence suggests that aerobic glycolysis is related to the progression of oral squamous cell carcinoma (OSCC). Hence, we focused on glycolysis-related gene sets to screen for potential therapeutic targets for OSCC. The expression profiles of OSCC samples and normal controls were obtained from The Cancer Genome Atlas (TCGA). Then, the differentially expressed gene sets were selected from the official GSEA website following extraction of the differentially expressed core genes (DECGs). Subsequently, we tried to build a risk model on the basis of DECGs to predict the prognosis of OSCC patients via Cox regression analysis. Furthermore, crucial glycolysis-related genes were selected to explore their biological roles in OSCC. Two active glycolysis-related pathways were acquired and 66 DECGs were identified. Univariate Cox regression analysis showed that six genes, including HMMR, STC2, DDIT4, DEPDC1, SLC16A3, and AURKA, might be potential prognostic factors. Subsequently, a risk formula consisting of DEPDC1, DDIT4, and SLC16A3 was established on basis of the six molecules. Furthermore, DEPDC1 was proven to be related to advanced stage cancer and lymph node metastasis. Moreover, functional experiments suggested that DEPDC1 promoted the aerobic glycolysis, migration, and invasion of OSCC via the WNT/β-catenin pathway. The risk score according to glycolysis-related gene expression might be an independent prognostic factor in OSCC. In addition, DEPDC1 was identified as playing a carcinogenic role in OSCC progression, suggesting that DEPDC1 might be a novel biomarker and therapeutic target for OSCC.
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Bin, 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.
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Background. Immune microenvironment implicated in liver cancer development. Nevertheless, previous studies have not fully investigated the immune microenvironment in liver cancer. Methods. The open-access data used for analysis were obtained from The Cancer Genome Atlas (TCGA-LIHC) and the International Cancer Genome Consortium databases (ICGC-JP and ICGC-FR). R program was employed to analyze all the data statistically. Results. First, the TCGA-LIHC, ICGC-FR, and ICGC-JP cohorts were selected for our analysis, which were merged into a combined cohort. Then, we quantified 53 immune terms in this combined cohort with large populations using the ssGSEA algorithm. Next, a prognostic approach was established based on five immune principles (CORE.SERUM.RESPONSE.UP, angiogenesis, CD8.T.cells, Th2.cells, and B.cells) was established, which showed great prognostic prediction efficiency. Clinical correlation analysis demonstrated that high-risk patients could reveal higher progressive clinical features. Next, to examine the inherent biological variations in high- and low-risk patients, pathway enrichment tests were conducted. DNA repair, E2F targets, G2M checkpoints, HEDGEHOG signaling, mTORC1 signaling, and MYC target were positively correlated with the risk score. Examination of genomic instability revealed that high-risk patients may exhibit a higher tumor mutation burden score. Meanwhile, the risk score showed a strong positive correlation with the tumor stemness index. In addition, the Tumor Immune Dysfunction and Exclusion outcome indicated that high-risk patients could be higher responsive to immunotherapy, whereas low-risk patients may be higher responsive to Erlotinib. Finally, six characteristic genes DEPDC1, DEPDC1B, NGFR, CALCRL, PRR11, and TRIP13 were identified for risk group prediction. Conclusions. In summary, our study identified a signature as a useful tool to indicate prognosis and therapy options for liver cancer patients.
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Pang, 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.
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Gastrointestinal stromal tumors (GISTs) are the most common human sarcoma and are initiated by activating mutations in the KIT or PDGFRA receptor tyrosine kinases. Chromosome 22q deletions are well-recognized frequent abnormalities in GISTs, occurring in ∼50% of GISTs. These deletions are thought to contribute to the pathogenesis of this disease via currently unidentified tumor suppressor mechanisms. Using whole exome sequencing, we report recurrent genomic inactivated DEPDC5 gene mutations in GISTs (16.4%, 9 of 55 patients). The demonstration of clonal DEPDC5 inactivation mutations in longitudinal specimens and in multiple metastases from individual patients suggests that these mutations have tumorigenic roles in GIST progression. DEPDC5 inactivation promotes GIST tumor growth in vitro and in nude mice. DEPDC5 reduces cell proliferation through the mTORC1-signaling pathway and subsequently induces cell-cycle arrest. Furthermore, DEPDC5 modulates the sensitivity of GIST to KIT inhibitors, and the combination therapy with mTOR inhibitor and KIT inhibitor may work better in GIST patients with DEPDC5 inactivation. These findings of recurrent genomic alterations, together with functional data, validate the DEPDC5 as a bona fide tumor suppressor contributing to GIST progression and a biologically relevant target of the frequent chromosome 22q deletions.
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Motomura, 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.
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Purpose. Genetic polymorphisms of MICA and DEPDC5 have been reported to correlate with progression to hepatocellular carcinoma (HCC) in chronic hepatitis C patients. However, correlation of these genetic variants with HCC recurrence following hepatectomy has not yet been clarified. Methods. Ninety-six consecutive HCC patients who underwent hepatectomy, including 64 patients who were hepatitis C virus (HCV) positive, were genotyped for MICA (rs2596542) and DEPDC5 (rs1012068). Recurrence-free survival rates (RFS) were compared for each genotype. Results. Five-year HCC recurrence-free survival (RFS) rates following hepatectomy were 20.7% in MICA GG allele carriers, 38.7% in GA, and 20.8% in AA, respectively (P=0.72). The five-year RFS rate was 23.8% in DEPDC5 TT allele carriers and 31.8% in TG/GG, respectively (P=0.47). The survival rates in all (including HCV-negative) patients were also similar among each MICA and DEPDC5 genotype following hepatectomy. Among HCV-positive patients carrying the DEPDC5 TG/GG allele, low fibrosis stage (F0-2) occurred more often compared with TT carriers (P<0.05). Conclusions. Neither MICA nor DEPDC5 genetic polymorphism correlates with HCC recurrence following hepatectomy. DEPDC5 minor genotype data suggest a high susceptibility for HCC development in livers, even those with low fibrosis stages.
Dissertations / Theses on the topic "DEPDC1A"
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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.
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2011/2012Metastasis 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
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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.
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The identification of universal tumor-specific antigens (TSA) shared between multiple patients and/or multiple tumors is of great importance to overcome the practical limitations of personalized cancer immunotherapy. Recent studies support the involvement of DEPDC1 in many aspects of cancer traits, such as cell proliferation, anti-apoptosis and cell invasion, suggesting that it may play key roles in the oncogenic process. In this study, we report that DEPDC1 expression is up-regulated in several types of human tumors, and closely linked to a poorer prognosis; therefore, it might be regarded as a novel universal oncoantigen potentially suitable for targeting many different cancers. In this regard, we report the identification of an immunogenic DEPDC1-derived epitope restricted for the HLA-A*0201 molecule, which is able to induce cytotoxic T lymphocytes (CTL) exerting a strong and specific functional response in vitro in response not only to peptide-loaded cells but also to triple negative breast cancer (TNBC) cells endogenously expressing the DEPDC1 protein. Such CTL are also therapeutically active against human TNBC xenografts in vivo upon adoptive transfer in immunodeficient mice. Overall, these data provide evidences that this DEPDC1-derived antigenic epitope can be exploited as a new tool for the development of immunotherapeutic strategies for HLA-A*0201 patients with TNBC, and potentially many other cancers. Moreover, we plan to employ an approach of multiplexing digital pathology to study the intimate relationships that adoptively transferred lymphocytes can establish with TNBC cells in tumor-bearing mice, as further advances in immunotherapy approaches require a detailed understanding of cell dynamics within the tumor microenvironment. The benefits of multispectral immunohistochemistry, combined with the development of software for quantitation, are making this methodology an increasingly powerful tool in the analysis and characterization of tissue and cellular processes, supporting diagnostic potential in order to improve therapies.L’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.
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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.
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One of the most frequent alterations occurring in cancer is the inactivation of the mechanisms controlling cell cycle progression: the cellular checkpoints. Among the different existing checkpoints, the one controlling the G2/M transition holds great interest because of its implications for genome stability and tumorigenesis.
Previous work in our lab identified DEPDC-1B as an E1A-induced gene during cell-cycle re-entry of differentiated cells (Nicassio et al. 2005). In this study, DEPDC-1B was found a cell cycle regulated-gene, with transcriptional expression peaking at the G2 and M phases (Nicassio et al. 2005). The DEPDC-1B protein possesses the structural features of a signaling protein, with two conserved domains (a DEP and a Rho-GAP domain) putatively involved in RhoGTPase signaling. Therefore, we hypothesized the existence of a previously un-described signaling pathway involving both DEPDC-1B and Rho-GTPases in the control of G2/M transition.
Our results identify DEPDC-1B as a key player in the regulation of mitotic entry in vertebrates. DEPDC-1B ablation causes a delay in mitotic entry in human cell lines and impairs mitotic progression in vivo during the early stages of Zebrafish development. By the use of biochemical and genetic approaches we provide evidence for a DEPDC- 1B/RhoA complex, possibly with the participation of the focal adhesion-specific receptor phosphatase PTPRF, able to regulate focal adhesion and cytoskeleton dynamics at the G2/M transition. Our model suggests that DEPDC-1B acts as a negative modulator of RhoA activity, and requires both the DEP and Rho-GAP domains, although the latter appears to be an atypical Rho-GAP that does not possess any GAP activity per se. We observed that, even in Zebrafish development, DEPDC-1B control on cell cycle progression is RhoA-dependent and involves both domains of DEPDC1B.
Our results also indicate that alterations of adhesion during the G2 phase occur as a
consequence of either DEPDC-1B/PTPRF silencing or RhoA hyper-activation. Such modulation of expression of the three genes is able to induce a delay in the G2/M transition. We, therefore, suggest the existence of an “Adhesion Checkpoint”, centered on the DEPDC-1B/RhoA axis, which controls cell detachment at the G2/M transition by the coordinated disassembly of focal adhesive structures. This previously uncharacterized mechanism appears to be essential for the proper progression to mitosis in vitro and in vivo and might potentially impact also on the mechanisms controlling DNA damage response at the G2/M phase and cellular transformation.
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DE, 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.
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DEP-domain containing 5 (DEPDC5) is part of the GATOR1 complex that functions as key inhibitor of the mechanistic target of rapamycin complex 1 (mTORC1) in the absence of amino acids. Mutations in DEPDC5 have been identified as the most common cause of either lesional or non-lesional focal epilepsy and are associated with mTOR hyperactivity. Recently, it has been hypothesized that somatic “second-hit” mutations occur in the brain of patients with the more severe symptomatology, including focal cortical dysplasia type II, drug-resistant epilepsy and intellectual disability. However, the mechanisms underlying dysplastic and epileptic phenotype following DEPDC5 loss-of-function, especially at the cellular levels, are still largely unknown, particularly regarding the morpho-functional impact of DEPDC5 deficiency at level of synaptic connectivity and transmission. The scope of my PhD project is to investigate the pathological changes occurring with DEPDC5 loss-of-function, with particular emphasis on cellular and synaptic morphology and physiology, and to address the role of the loss of heterozygosity in DEPDC5-related pathogenesis. As the full knockout of Depdc5 is embryonically lethal in rodents, in this study I have first characterized a heterozygous knockout mouse (Depdc5+/-), which failed to recapitulate the major phenotypic tracts of the pathology, except for a reduced PTZ-induced epileptic threshold. Therefore, to uncover the phenotype induced by Depdc5 loss-of-function, I have compared the condition of the constitutive Depdc5+/- haploinsufficent mouse with the more effective acute neuronal knockdown of Depdc5 by RNA interference. While heterozygous Depdc5+/- neurons have a very mild phenotype with morpho-functional features that are not significantly different from wild type neurons, acutely knocked down neurons exhibit a much stronger phenotype characterized by mTOR hyperactivation, increased soma size and dendritic arborization, increased excitatory synaptic transmission and intrinsic excitability of excitatory neurons, leading to an excitation/inhibition imbalance. These results uncover a novel synaptic phenotype that is causally linked to acute Depdc5 knockdown and mTOR hyperactivity, highlighting the loss of heterozygosity as causal factor for the establishment of FCD-related neuronal phenotype, and suggesting an involvement of Depdc5 in the neurodevelopmental processes. The robust synaptic phenotype resulting from acute sh-mediated, but not constitutive, Depdc5 deficiency is reminiscent of the somatic second-hit mechanism in patients with focal cortical dysplasia and, together with the increased intrinsic excitability, can trigger the epileptogenic process.
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CERULLO, 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.
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Focal Epilepsy (FE) accounts for more than the half of the total cases of all epileptic syndrome, around 60%. It can be caused by either genetic or acquired factors, such as brain trauma, tumors or inflammation. However, it is widely recognized to have a mostly a genetic basis. Mutations at the level of the GATOR1 complex components, DEPDC5, NPRL2 and NPRL3, were found in patients with FE, confirming the key role of the GATOR1 complex in the pathogenesis of various FE syndromes. In particular, it has been discovered that mutations of DEPDC5 gene are implicated in the 5%–37% of a broad range of FEs, both lesional or non-lesional and are associated with mTOR hyperactivity. The specific mechanism underlying the epileptogenic phenotype following DEPDC5 loss is far from being clear. The aim of this thesis is to deepen the impact of Depdc5 loss-of-function at the cellular level, by focusing the attention on synaptic transmission and plasticity. In order to overcome the problem of embryonic lethality of Depdc5 full knockout in rodents, and the failure of Depdc5 constitutive heterozygous knockout mice to recapitulate the major epileptogenic traits, we used Depdc5-floxed mice and applied the Cre/LoxP technique to generate a model of Depdc5 cKO. We transfected primary cortical neurons obtained from Depdc5-floxed mice with lentiviruses expressing either active or inactive Cre recombinase and performed electrophysiological and biochemical experiments. We observed an increased in excitatory synaptic transmission and intrinsic excitability, while no difference occurred at the level of the inhibitory synaptic transmission. Given the involvement of mTOR in the mechanism of plasticity and the effect of its dysregulation on synaptic transmission, we assessed whether Depdc5 loss could also have an impact at the level of the short-term plasticity (STP). However, no effects were found at the level of either excitatory or inhibitory synaptic transmission. The data suggest that Depdc5 loss mostly induces a strengthening of excitatory transmission at the post-synaptic level and by increasing the number of connections, without directly affecting pre-synaptic mechanisms. Thus, the enhanced excitatory synaptic transmission and increased intrinsic excitability could generate a synergistic effect underlying the excitation/inhibition imbalance that triggers the epileptogenic process.
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Motta, 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.
Full textAbstract:
BACKGROUND E SCOPO
L’epatocarcinoma (HCC) rappresenta la terza causa di mortalità per tumore. Il principale fattore di rischio è determinato dalla presenza di malattia epatica avanzata, in particolare legata ad infezioni virali croniche, tra cui HCV predomina nel bacino mediterraneo. Esistono forti differenze di suscettibilità individuale legata a fattori genetici.
Due studi di associazione genome-wide (GWAS) hanno identificato un’associazione tra i geni DEP domain containing 5 (DEPDC5) e MHC class I polypeptide-related sequence A (MICA) e il epatocarcinoma (HCC) in soggetti asiatici con infezione cronica da virus dell’epatite C (CHC). Dato che il background genetico varia tra soggetti di differente origine etnica, e che il dato non è ancora stato replicato indipendentemente, lo scopo di questo lavoro è stato quello di analizzare l’effetto dei polimorfismi rs2596542 di MICA e rs1012068 di DEPDC5 sul rischio di HCC e fibrosi epatica in una casistica di soggetti di origine europea con infezione cronica da HCV.
METODI
Le varianti genetiche (polimorfismi rs2596542 di MICA e rs1012068 di DEPDC5) sono state genotipizzate in una coorte italiana di individui con CHC: soggetti con epatocarcinoma (n=149), controlli con cirrosi senza epatocarcinoma (controllo per predisposizione alla cancerogenesi epatica; n=145), e controlli con CHC senza fibrosi significativa (controlli per predisposizione alla fibrogenesi; n=169). Le associazioni significative sono state in seguito validate in una casistica indipendente tedesca, che presentava uno spettro completo di malattia epatica (=299): soggetti con epatocarcinoma (n=67), controlli con fibrosi significativa (n=144), e controlli senza fibrosi significativa (n=88).
RISULTATI
Nella casistica italiana, le varianti di MICA o DEPDC5 non sono risultate associate con HCC. Tuttavia, è stato osservato un aumentato rischio di cirrosi epatica nel gruppo di soggetti portatori dell’allele G della variante rs1012068 di DEPDC5 nella coorte italiana (OR=1.46; 95% CI=1.04-2.04; p=0.027), e l’associazione con fibrosi avanzata è stata replicata nella coorte tedesca di validazione (OR=1.57; 95% CI=1.14-2.16; p=0.006).
CONCLUSIONI
In questo studio, non abbiamo replicato l’associazione tra le varianti rs2596542 di MICA e rs1012068 di DEPDC5 con HCC HCV-correlato in europei. Tuttavia, il polimorfismo rs1012068 è stato identificato come fattore di rischio per fibrosi severa, il principale fattore di rischio per HCC, in europei con infezione cronica da HCV.Background 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.
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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.
Full textAbstract:
Pour analyser les mécanismes pathogéniques de la mutation de SQSTM1 dans la SLA, nous avons développé un modèle d’haploinsuffisance de sqstm1 chez le poisson zèbre. La perte de fonction de ce gène induit un phénotype moteur caractéristique de la SLA. Pour élucider les mécanismes entraînant la dégénérescence des motoneurones dans cette maladie, nous avons étudié les interactions épistatiques de c9orf72 et de sqstm1 chez le poisson zèbre et nous avons observé que les deux protéines appartiennent à une voie cellulaire commune, avec c9orf72 agissant en aval de sqstm1. Dans des cultures primaires de motoneurones de souris, nous avons démontré que la perte de ces gènes entraîne la mort des motoneurones associée à des défauts de l’autophagie. Afin de développer un modèle qui récapitulerait les différents mécanismes de la mutation de C9ORF72 dans la SLA, nous avons combiné l’inhibition partielle de ce gène avec l’expression des DPRs chez le poisson zèbre. Cela induit un phénotype moteur caractérisé par des défauts locomoteurs et une paralysie. En particulier, nous avons observé que les répétitions de GP s’accumulent lorsque c9orf72 est inhibé. Ceci est associé à une accumulation de SQSTM1/p62 ainsi qu’à la perte des motoneurones. Ces phénotypes sont limités lors de l’inhibition de la caspase 9, un régulateur essentiel de l’apoptose. De plus, en activant l’autophagie avec la rapamycine, nous avons amélioré la clairance des GP et de p62, restaurant ainsi les paramètres moteurs. Ces résultats montrent que la toxicité des DPRs est relative au niveau de de l’expression de C9ORF72, suggérant que le gain et la perte de fonction synergisent dans la pathogénicité de C9ORF72To 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
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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.
Full textAbstract:
碩士國立陽明大學
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.
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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.
Full textAbstract:
碩士國立陽明大學
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.
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Wilson, Jasmine Joy. "DEPDC5 is a metabolic checkpoint regulator in the B cell AA-mTORC1 pathway." Thesis, 2020. http://hdl.handle.net/2440/128586.
Full textAbstract:
Immunometabolism is a rapidly developing field that is central to understanding the homeostatic maintenance and induction of immune responses. Naïve B cells rest in quiescent states until antigen (Ag) is encountered, which simultaneously triggers a metabolic switch enabling enhanced growth, proliferation and differentiation in activated B cells. Central to this metabolic activation is the mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) pathway, which is required for multiple inputs to determine if sufficient nutrients are available to drive these metabolic programs. In recent years amino acid (AA) sensing and availability have been shown to be important for the control of mTORC1 in various cell types, however their importance in B cell metabolism was largely unknown. DEPDC5 is a metabolic checkpoint protein that mediates crosstalk between AA availability and the mTORC1 pathway, but it’s role in B cells has not been explored. The results in this thesis showed that Depdc5 is expressed in B cells and most abundantly in germinal center (GC) B cells (GCB). A novel line of conditional knock-out mice was generated that lack DEPDC5 in mature B cells (Depdc5flox/flox x Cd23Cre). This deletion led to constitutive mTORC1 activation in mature B cells. Analysis of Depdc5flox/flox x Cd23Cre mice showed no impairment of B cell development and at homeostasis, mature B cell frequencies were unchanged from controls. Despite this, mature B cells in resting mice that lacked B cell expression of DEPDC5 exhibited a hyperactive phenotype with increased mTOR signalling, increased biomass and higher levels of expression of B cell activation markers. The effects of DEPDC5 deletion in B cells became more apparent in challenged animals. Fewer GC B cells were present in draining LNs following viral infection than in littermate controls. Furthermore, the absence of Depdc5 in B cells led to reduced generation of anti-viral IgM Ab, but not antiviral IgG, and impaired affinity maturation in a protein immunisation model. Mechanistically it was shown that DEPDC5 was required to protect GC B cells from late-stage apoptosis and restrain B cell proliferation following viral infection. Thus, Depdc5 was required to ensure the sustained expansion of GC B cells in humoral immune responses, likely by restraining their metabolic activity in response to the limited nutrient microenvironment in the GC. However, in contrast, an increase GC B cells frequency and number was also observed in the lung of Depdc5-deficient mice following IAV infection. Furthermore, DEPDC5 was observed to be dispensable in B cell activation within GALT-associated chronic GCs. These results broaden understanding of AA responsive metabolic checkpoint regulators and have implications for nutritional control of optimal humoral responses. Thus, this study contributed to broadening the understanding of how metabolic pathways shape immunity in health and disease.Thesis (Ph.D.) -- University of Adelaide, School of Biological Sciences, 2020
Books on the topic "DEPDC1A"
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Tantiwiramanond, Darunee. Development and Education Program for Daughters and Communities Center (DEPDC). Bangkok, Thailand: Women's Action and Resource Initiative, 1996.
Find full textBook chapters on the topic "DEPDC1A"
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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.
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"Depdc2." In Encyclopedia of Signaling Molecules, 1352. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_100971.
Full textConference papers on the topic "DEPDC1A"
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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.
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Padi, 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.
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Sharma, 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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