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Article ; Online: Transcriptional Regulation of Cell-Type-Enriched Genes during Development in Dictyostelium discoideum Analyzed by Nuclear Run-On Assays: (Dictyostelium discoideum/cell differentiation/cell-type-enriched genes/nuclear run-on assay).

Morio, Takahiro / Ozaki, Toshinori / Takeuchi, Ikuo / Tasaka, Masao

2023 Volume 33, Issue 4, Page(s) 293–298

Abstract: We have previously isolated several cell-type-enriched mRNAs of Dictyostelium discoideum. Since the temporal pattern of appearance and cell-type-enrichment of these RNAs were examined only by determining their accumulation, it was unclear whether their ... ...

Abstract	We have previously isolated several cell-type-enriched mRNAs of Dictyostelium discoideum. Since the temporal pattern of appearance and cell-type-enrichment of these RNAs were examined only by determining their accumulation, it was unclear whether their accumulation is regulated at the transcription level or the post-transcriptional level. To distinguish between these two possibilities, we examined the temporal and cell-type-enriched transcription of several of these genes by nuclear run-on assay. The results suggest that some genes are controlled in both temporal accumulation and cell-type-enrichment at the transcriptional level, but post-transcriptional regulation is also important for regulating cell-type enrichment in the case of some other genes.
Language	English
Publishing date	2023-06-06
Publishing country	Japan
Document type	Journal Article
ZDB-ID	280433-5
ISSN	1440-169X ; 0012-1592
ISSN (online)	1440-169X
ISSN	0012-1592
DOI	10.1111/j.1440-169X.1991.00293.x
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Zs.A 194: Show issues

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Article ; Online: The role of circular RNA during the urological cancer metastasis: exploring regulatory mechanisms and potential therapeutic targets.

Xu, Yan / Gao, Zhipeng / Sun, Xiaoyu / Li, Jun / Ozaki, Toshinori / Shi, Du / Yu, Meng / Zhu, Yuyan

Cancer metastasis reviews

2024

Abstract: Metastasis is a major contributor to treatment failure and death in urological cancers, representing an important biomedical challenge at present. Metastases form as a result of cancer cells leaving the primary site, entering the vasculature and ... ...

Abstract	Metastasis is a major contributor to treatment failure and death in urological cancers, representing an important biomedical challenge at present. Metastases form as a result of cancer cells leaving the primary site, entering the vasculature and lymphatic vessels, and colonizing clones elsewhere in the body. However, the specific regulatory mechanisms of action underlying the metastatic process of urological cancers remain incompletely elucidated. With the deepening of research, circular RNAs (circRNAs) have been found to not only play a significant role in tumor progression and prognosis but also show aberrant expression in various tumor metastases, consequently impacting tumor metastasis through multiple pathways. Therefore, circRNAs are emerging as potential tumor markers and treatment targets. This review summarizes the research progress on elucidating how circRNAs regulate the urological cancer invasion-metastasis cascade response and related processes, as well as their role in immune microenvironment remodeling and circRNA vaccines. This body of work highlights circRNA regulation as an emerging therapeutic target for urological cancers, which should motivate further specific research in this regard.
Language	English
Publishing date	2024-04-01
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	604857-2
ISSN	1573-7233 ; 0167-7659
ISSN (online)	1573-7233
ISSN	0167-7659
DOI	10.1007/s10555-024-10182-x
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Zs.A 1812: Show issues

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Article: p53-Armed Oncolytic Virotherapy Improves Radiosensitivity in Soft-Tissue Sarcoma by Suppressing BCL-xL Expression.

Komatsubara, Tadashi / Tazawa, Hiroshi / Hasei, Joe / Omori, Toshinori / Sugiu, Kazuhisa / Mochizuki, Yusuke / Demiya, Koji / Yoshida, Aki / Fujiwara, Tomohiro / Kunisada, Toshiyuki / Urata, Yasuo / Kagawa, Shunsuke / Ozaki, Toshifumi / Fujiwara, Toshiyoshi

Acta medica Okayama

2024 Volume 78, Issue 2, Page(s) 151–161

Abstract: Soft-tissue sarcoma (STS) is a heterogeneous group of rare tumors originating predominantly from the embryonic mesoderm. Despite the development of combined modalities including radiotherapy, STSs are often refractory to antitumor modalities, and novel ... ...

Abstract	Soft-tissue sarcoma (STS) is a heterogeneous group of rare tumors originating predominantly from the embryonic mesoderm. Despite the development of combined modalities including radiotherapy, STSs are often refractory to antitumor modalities, and novel strategies that improve the prognosis of STS patients are needed. We previously demonstrated the therapeutic potential of two telomerase-specific replication-competent oncolytic adenoviruses, OBP-301 and tumor suppressor p53-armed OBP-702, in human STS cells. Here, we demonstrate in vitro and in vivo antitumor effects of OBP-702 in combination with ionizing radiation against human STS cells (HT1080, NMS-2, SYO-1). OBP-702 synergistically promoted the antitumor effect of ionizing radiation in the STS cells by suppressing the expression of B-cell lymphoma-X large (BCL-xL) and enhancing ionizing radiation-induced apoptosis. The in vivo experiments demonstrated that this combination therapy significantly suppressed STS tumors' growth. Our results suggest that OBP-702 is a promising antitumor reagent for promoting the radiosensitivity of STS tumors.
MeSH term(s)	Sarcoma/therapy ; Sarcoma/radiotherapy ; Humans ; Oncolytic Virotherapy/methods ; bcl-X Protein/genetics ; bcl-X Protein/metabolism ; Radiation Tolerance ; Cell Line, Tumor ; Animals ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Mice ; Apoptosis ; Adenoviridae/genetics
Chemical Substances	bcl-X Protein ; Tumor Suppressor Protein p53 ; BCL2L1 protein, human
Language	English
Publishing date	2024-04-30
Publishing country	Japan
Document type	Journal Article
ZDB-ID	188415-3
ISSN	0386-300X ; 0001-6152
ISSN	0386-300X ; 0001-6152
DOI	10.18926/AMO/66924
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Ua VI Zs.421: Show issues

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Article ; Online: Correction: Ishihara et al. Association between Daily Physical Activity and Locomotive Syndrome in Community-Dwelling Japanese Older Adults: A Cross-Sectional Study.

Ishihara, Yoshihiko / Ozaki, Hayao / Nakagata, Takashi / Yoshihara, Toshinori / Natsume, Toshiharu / Kitada, Tomoharu / Ishibashi, Masayoshi / Deng, Pengyu / Yamada, Yasuyuki / Kobayashi, Hiroyuki / Machida, Shuichi / Naito, Hisashi

International journal of environmental research and public health

2023 Volume 20, Issue 18

Abstract: There was an error in the " ...

Abstract	There was an error in the "
Language	English
Publishing date	2023-09-13
Publishing country	Switzerland
Document type	Published Erratum
ZDB-ID	2175195-X
ISSN	1660-4601 ; 1661-7827
ISSN (online)	1660-4601
ISSN	1661-7827
DOI	10.3390/ijerph20186751
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Article ; Online: HES1-mediated down-regulation of miR-138 sustains NOTCH1 activation and promotes proliferation and invasion in renal cell carcinoma.

Liu, Shuangjie / Dou, Lei / Miao, Miao / Man, Xiaojun / Wei, Baojun / Jiang, Zhaowei / Ouyang, Yongze / Ozaki, Toshinori / Yu, Meng / Zhu, Yuyan

Journal of experimental & clinical cancer research : CR

2023 Volume 42, Issue 1, Page(s) 72

Abstract: Background: Although the aberrant activation of NOTCH1 pathway causes a malignant progression of renal cell carcinoma (RCC), the precise molecular mechanisms behind the potential action of pro-oncogenic NOTCH1/HES1 axis remain elusive. Here, we examined ...

Abstract	Background: Although the aberrant activation of NOTCH1 pathway causes a malignant progression of renal cell carcinoma (RCC), the precise molecular mechanisms behind the potential action of pro-oncogenic NOTCH1/HES1 axis remain elusive. Here, we examined the role of tumor suppressive miR-138-2 in the regulation of NOTCH1-HES1-mediated promotion of RCC. Methods: This study employed bioinformatics, xenotransplant mouse models, ChIP assay, luciferase reporter assay, functional experiments, real-time PCR and Western blot analysis to explore the mechanisms of miR-138-2 in the regulation of NOTCH1-HES1-mediated promotion of RCC, and further explored miR-138-2-containing combination treatment strategies. Results: There existed a positive correlation between down-regulation of miR-138 and the aberrant augmentation of NOTCH1/HES1 regulatory axis. Mechanistically, HES1 directly bound to miR-138-2 promoter region and thereby attenuated the transcription of miR-138-5p as well as miR-138-2-3p. Further analysis revealed that miR-138-5p as well as miR-138-2-3p synergistically impairs pro-oncogenic NOTCH1 pathway through the direct targeting of APH1A, MAML1 and NOTCH1. Conclusions: Collectively, our current study strongly suggests that miR-138-2 acts as a novel epigenetic regulator of pro-oncogenic NOTCH1 pathway, and that the potential feedback regulatory loop composed of HES1, miR-138-2 and NOTCH1 contributes to the malignant development of RCC. From the clinical point of view, this feedback regulatory loop might be a promising therapeutic target to treat the patients with RCC.
MeSH term(s)	Animals ; Humans ; Mice ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/metabolism ; Cell Line, Tumor ; Cell Proliferation ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Kidney Neoplasms/genetics ; Kidney Neoplasms/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Receptor, Notch1/genetics ; Receptor, Notch1/metabolism ; Transcription Factor HES-1/genetics ; Transcription Factor HES-1/metabolism
Chemical Substances	Hes1 protein, mouse ; MicroRNAs ; Receptor, Notch1 ; Transcription Factor HES-1 ; Notch1 protein, mouse
Language	English
Publishing date	2023-03-28
Publishing country	England
Document type	Journal Article
ZDB-ID	803138-1
ISSN	1756-9966 ; 0392-9078
ISSN (online)	1756-9966
ISSN	0392-9078
DOI	10.1186/s13046-023-02625-0
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Zs.A 2065: Show issues

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Article ; Online: Oridonin inhibits bladder cancer survival and immune escape by covalently targeting HK1.

Liu, Shuangjie / Wang, Xialu / Sun, Xiaojie / Wei, Baojun / Jiang, Zhaowei / Ouyang, Yongze / Ozaki, Toshinori / Yu, Meng / Liu, Yongxiang / Zhang, Rong / Zhu, Yuyan

Phytomedicine : international journal of phytotherapy and phytopharmacology

2024 Volume 126, Page(s) 155426

Abstract: Background: Hexokinase I (HK1) is highly expressed in a variety of malignancies, regulates glycolytic pathway in cancer cells, and thus considered to be one of the promising molecular targets for cancer therapy. Nonetheless, the development of a ... ...

Abstract	Background: Hexokinase I (HK1) is highly expressed in a variety of malignancies, regulates glycolytic pathway in cancer cells, and thus considered to be one of the promising molecular targets for cancer therapy. Nonetheless, the development of a specific inhibitor against HK1 remains elusive. Purpose: This study aims to elucidate the mechanism by which oridonin inhibits the proliferation and immune evasion of bladder cancer cells, specifically through the suppression of HK1. Methods: To examine the mechanisms by which oridonin directly binds to cysteines of HK1 and inhibits bladder cancer growth, this study utilized a variety of methods. These included the Human Proteome Microarray, Streptavidin-agarose affinity assay, Biolayer Interferometry (BLI) ainding analysis, Mass Spectrometry, Cellular Thermal Shift Assay, Extracellular Acidification Rate measurement, and Xenotransplant mouse models. Results: As indicated by our current findings, oridonin forms a covalent bond with Cys-813, located adjacently to glucose-binding domain of HK1. This suppresses the enzymatic activity of HK1, leading to an effective reduction of glycolysis, which triggers cell death via apoptosis in cells derived from human bladder cancer. Significantly, oridonin also inhibits lactate-induced PD-L1 expression in bladder cancer. Furthermore, pairing oridonin with a PD-L1 inhibitor amplifies the cytotoxicity of CD8+ T cells against bladder cancer. Conclusion: This research strongly suggests that oridonin serves as a covalent inhibitor of HK1. Moreover, it indicates that functional cysteine residue of HK1 could operate as viable targets for selective inhibition. Consequently, oridonin exhibits substantial potential for the evolution of anti-cancer agents targeting the potential therapeutic target HK1 via metabolism immunomodulation.
MeSH term(s)	Animals ; Mice ; Humans ; Cell Line, Tumor ; Urinary Bladder Neoplasms/drug therapy ; Diterpenes, Kaurane/pharmacology ; Diterpenes, Kaurane/chemistry ; Antineoplastic Agents/pharmacology ; Cell Proliferation ; Apoptosis
Chemical Substances	oridonin (0APJ98UCLQ) ; Diterpenes, Kaurane ; Antineoplastic Agents
Language	English
Publishing date	2024-02-07
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1205240-1
ISSN	1618-095X ; 0944-7113
ISSN (online)	1618-095X
ISSN	0944-7113
DOI	10.1016/j.phymed.2024.155426
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Zs.A 4115: Show issues

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Article: Anoxification recovery using underwater LED irradiation and influence of its optical spectrum on water quality improvement

Honglikith, Daoluang / Harada, Masayoshi / Hiramatsu, Kazuaki / Tabata, Toshinori / Ozaki, Akinori

Paddy and water environment. 2022 Jan., v. 20, no. 1

2022

Abstract: This study focuses on a method for improving water quality via anoxification recovery using underwater LED treatment in an organically polluted reservoir. The main aim was to evaluate the effects of the optical spectrum and light intensity of LED ... ...

Abstract	This study focuses on a method for improving water quality via anoxification recovery using underwater LED treatment in an organically polluted reservoir. The main aim was to evaluate the effects of the optical spectrum and light intensity of LED irradiation on the maintenance of healthy aerobic conditions, as well as anoxification recovery, by promoting oxygen production via phytoplankton photosynthesis. Water quality was monitored via beaker and water tank experiments while using LED irradiation for 24 h (12 h on/12 h off) for 2 months in anoxic water, where the anaerobic decomposition of organic matter progressed under strong reductive conditions. As a result, red–green–blue (RGB) light was advantageous for promoting rapid oxygen production by phytoplankton photosynthesis compared with the mixed red and blue light. In particular, LED irradiation, including the green color, preserved the healthy dissolved oxygen environment without lowering the oxygen level in the dark. In addition, RGB irradiation (R:B:G = 1:1:1) did not only assist in preserving a healthy aerobic state in spite of low light intensities but also evidently decreased concentrations of total nitrogen and total phosphorous. In conclusion, the spatial effect of water quality improvement via LED irradiation was not limited to the vicinity of the light source but was applicable to a wide range, in which the light intensity contributed to one-fifth of the optimum photon intensity for phytoplankton photosynthesis.
Keywords	blue light ; color ; dissolved oxygen ; irradiation ; light intensity ; organic matter ; oxygen ; oxygen production ; paddies ; phosphorus ; photons ; photosynthesis ; phytoplankton ; total nitrogen ; water ; water quality
Language	English
Dates of publication	2022-01
Size	p. 153-175.
Publishing place	Springer Singapore
Document type	Article
ZDB-ID	2168266-5
ISSN	1611-2490
ISSN	1611-2490
DOI	10.1007/s10333-021-00883-2
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Fluorescence-guided assessment of bone and soft-tissue sarcomas for predicting the efficacy of telomerase-specific oncolytic adenovirus.

Uotani, Koji / Tazawa, Hiroshi / Hasei, Joe / Fujiwara, Tomohiro / Yoshida, Aki / Yamakawa, Yasuaki / Omori, Toshinori / Sugiu, Kazuhisa / Komatsubara, Tadashi / Kondo, Hiroya / Morita, Takuya / Kiyono, Masahiro / Yokoo, Suguru / Hata, Toshiaki / Kunisada, Toshiyuki / Takeda, Ken / Urata, Yasuo / Fujiwara, Toshiyoshi / Ozaki, Toshifumi

PloS one

2024 Volume 19, Issue 2, Page(s) e0298292

Abstract: Bone and soft-tissue sarcomas are rare malignancies with histological diversity and tumor heterogeneity, leading to the lack of a common molecular target. Telomerase is a key enzyme for keeping the telomere length and human telomerase reverse ... ...

Abstract	Bone and soft-tissue sarcomas are rare malignancies with histological diversity and tumor heterogeneity, leading to the lack of a common molecular target. Telomerase is a key enzyme for keeping the telomere length and human telomerase reverse transcriptase (hTERT) expression is often activated in most human cancers, including bone and soft-tissue sarcomas. For targeting of telomerase-positive tumor cells, we developed OBP-301, a telomerase-specific replication-competent oncolytic adenovirus, in which the hTERT promoter regulates adenoviral E1 gene for tumor-specific viral replication. In this study, we present the diagnostic potential of green fluorescent protein (GFP)-expressing oncolytic adenovirus OBP-401 for assessing virotherapy sensitivity using bone and soft-tissue sarcomas. OBP-401-mediated GFP expression was significantly associated with the therapeutic efficacy of OBP-401 in human bone and soft-tissue sarcomas. In the tumor specimens from 68 patients, malignant and intermediate tumors demonstrated significantly higher expression levels of coxsackie and adenovirus receptor (CAR) and hTERT than benign tumors. OBP-401-mediated GFP expression was significantly increased in malignant and intermediate tumors with high expression levels of CAR and hTERT between 24 and 48 h after infection. Our results suggest that the OBP-401-based GFP expression system is a useful tool for predicting the therapeutic efficacy of oncolytic virotherapy on bone and soft-tissue sarcomas.
MeSH term(s)	Humans ; Adenoviridae/physiology ; Telomerase/genetics ; Telomerase/metabolism ; Fluorescence ; Adenoviridae Infections ; Oncolytic Virotherapy/methods ; Sarcoma/therapy ; Soft Tissue Neoplasms ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Cell Line, Tumor
Chemical Substances	Telomerase (EC 2.7.7.49) ; Green Fluorescent Proteins (147336-22-9)
Language	English
Publishing date	2024-02-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0298292
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Article: Mapping of new skin tumor susceptibility loci by a phenotype-driven congenic approach.

Fujiwara, Kyoko / Inagaki, Yoshinori / Soma, Masayoshi / Ozaki, Toshinori / Nagase, Hiroki

Oncology letters

2018 Volume 16, Issue 5, Page(s) 6670–6676

Abstract: As cancer susceptibility varies among mouse strains, mouse models are powerful tools for the identification of genes responsible for cancer development. Several cancer susceptibility loci have been mapped by genetic analysis using cancer-resistant and ... ...

Abstract	As cancer susceptibility varies among mouse strains, mouse models are powerful tools for the identification of genes responsible for cancer development. Several cancer susceptibility loci have been mapped by genetic analysis using cancer-resistant and cancer-susceptible mouse strains. However, only a few corresponding genes for these loci have been identified, because most of the cancer susceptibility loci are low-penetrance alleles. We reported previously that wild-derived PWK mice showed no tumor development on treatment with the two-stage skin carcinogenesis protocol [induced by 7.12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)], and that this phenotype is dominant-resistant when crossed with the highly susceptible strain FVB. From the analysis of the F1 backcross generation between PWK and FVB, we have mapped the new significant locus
Language	English
Publishing date	2018-09-24
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2573196-8
ISSN	1792-1082 ; 1792-1074
ISSN (online)	1792-1082
ISSN	1792-1074
DOI	10.3892/ol.2018.9495
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Article ; Online: CD133 prevents colon cancer cell death induced by serum deprivation through activation of Akt-mediated protein synthesis and inhibition of apoptosis.

Mori, Yusuke / Takeuchi, Ayaka / Miyagawa, Kengo / Yoda, Hiroyuki / Soda, Hiroaki / Nabeya, Yoshihiro / Watanabe, Naoko / Ozaki, Toshinori / Shimozato, Osamu

FEBS open bio

2021 Volume 11, Issue 5, Page(s) 1382–1394

Abstract: During the early phase of tumorigenesis, primary malignant cells survive within a low nutrition environment caused by a poorly organized vascular system. Here, we sought to determine the functional significance of CD133 in the survival of cancer cells ... ...

Abstract	During the early phase of tumorigenesis, primary malignant cells survive within a low nutrition environment caused by a poorly organized vascular system. Here, we sought to determine the functional significance of CD133 in the survival of cancer cells under nutrient-poor conditions. Knockdown and overexpression experiments demonstrated that CD133 suppresses colon cancer cell death induced by serum deprivation through activation of Akt-mediated anti-apoptosis and protein synthesis pathways. Furthermore, serum deprivation increased the amount of endogenous CD133 protein, which was regulated at least in part by phosphoinositide 3-kinase. Thus, it is highly likely that CD133 contributes to the acquisition/maintenance of the resistance to stress arising from nutrient deficiency in early avascular tumor tissues.
MeSH term(s)	AC133 Antigen/metabolism ; AC133 Antigen/physiology ; Apoptosis/physiology ; Carcinogenesis/genetics ; Carcinogenesis/metabolism ; Cell Death/genetics ; Cell Line, Tumor ; Cell Proliferation ; Cell Survival ; Colonic Neoplasms/genetics ; Colonic Neoplasms/metabolism ; Drug Resistance, Neoplasm ; Gene Expression/genetics ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Oncogene Protein v-akt/metabolism ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction
Chemical Substances	AC133 Antigen ; PROM1 protein, human ; Oncogene Protein v-akt (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2021-03-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2651702-4
ISSN	2211-5463 ; 2211-5463
ISSN (online)	2211-5463
ISSN	2211-5463
DOI	10.1002/2211-5463.13145
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