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Article: PHD finger protein 10 promotes cell proliferation by regulating CD44 transcription in gastric cancer.

Fan, Zhiyuan / Jiang, Xiao / Yan, Wenjing / Li, Jianfang / Yan, Min / Liu, Bingya / Yu, Beiqin

2024 Volume 10, Issue 7, Page(s) e29109

Abstract: PHD finger protein 10 (PHF10) plays an important role in the tumorigenesis of gastric cancer (GC). However, clinical significance and underlying molecular mechanisms about PHF10 is unclear. In the article, it suggested that PHF10 involved in tumor ... ...

Abstract	PHD finger protein 10 (PHF10) plays an important role in the tumorigenesis of gastric cancer (GC). However, clinical significance and underlying molecular mechanisms about PHF10 is unclear. In the article, it suggested that PHF10 involved in tumor progression and metastasis based on the analysis of datasets and 190 cases of tumor tissues in GC. And PHF10 provided the diagnostic value with areas under the receiver operating characteristics curve of 0.71 ± 0.069. Then we established GC cell lines MKN28 with PHF10 overexpression and SGC7901 with PHF10 knockdown. CCK8 assay and tumor xenograft experiment showed that upregulation of PHF10 could promote MKN28 cell proliferation, while PHF10 knockdown would inhibit the proliferation of SGC7901
Language	English
Publishing date	2024-04-03
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2024.e29109
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Regulation of pancreatic cancer metastasis through the Gli2-YAP1 axis via regulation of anoikis.

Yu, Beiqin / Gu, Dongsheng / Zhang, Xiaoli / Liu, Bingya / Xie, Jingwu

Genes & diseases

2022 Volume 9, Issue 6, Page(s) 1427–1430

Language	English
Publishing date	2022-05-24
Publishing country	China
Document type	Journal Article
ZDB-ID	2821806-1
ISSN	2352-3042 ; 2352-3042
ISSN (online)	2352-3042
ISSN	2352-3042
DOI	10.1016/j.gendis.2022.05.010
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Article: miR-29c inhibits metastasis of gastric cancer cells by targeting VEGFA.

Yu, Beiqin / Zhu, Nan / Fan, Zhiyuan / Li, Jianfang / Kang, Yani / Liu, Bingya

Journal of Cancer

2022 Volume 13, Issue 14, Page(s) 3566–3574

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2022-10-31
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2573318-7
ISSN	1837-9664
ISSN	1837-9664
DOI	10.7150/jca.77727
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Article ; Online: Blocking EGR1/TGF-β1 and CD44s/STAT3 Crosstalk Inhibits Peritoneal Metastasis of Gastric Cancer.

Jin, Yangbing / Wang, Chao / Zhang, Benyan / Sun, Ying / Ji, Jun / Cai, Qu / Jiang, Jinling / Zhang, Zhihao / Zhao, Liqin / Yu, Beiqin / Zhang, Jun

International journal of biological sciences

2024 Volume 20, Issue 4, Page(s) 1314–1331

Abstract: Peritoneal metastasis (PM) continues to limit the clinical efficacy of gastric cancer (GC). Early growth response 1 (EGR1) plays an important role in tumor cell proliferation, angiogenesis and invasion. However, the role of EGR1 derived from the tumor ... ...

Abstract	Peritoneal metastasis (PM) continues to limit the clinical efficacy of gastric cancer (GC). Early growth response 1 (EGR1) plays an important role in tumor cell proliferation, angiogenesis and invasion. However, the role of EGR1 derived from the tumor microenvironment in reshaping the phenotypes of GC cells and its specific molecular mechanisms in increasing the potential for PM are still unclear. In this study, we reported that EGR1 was significantly up-regulated in mesothelial cells from GC peritoneal metastases, leading to enhanced epithelial-mesenchymal transformation (EMT) and stemness phenotypes of GC cells under co-culture conditions. These phenotypes were achieved through the transcription and secretion of TGF-β1 by EGR1 in mesothelial cells, which could regulate the expression and internalization of CD44s. After being internalized into the cytoplasm, CD44s interacted with STAT3 to promote STAT3 phosphorylation and activation, and induced EMT and stemness gene transcription, thus positively regulating the metastasis of GC cells. Moreover, TGF-β1 secretion in the PM microenvironment was significantly increased compared with the matched primary tumor. The blocking effect of SHR-1701 on TGF-β1 was verified by inhibiting peritoneal metastases in xenografts. Collectively, the interplay of EGR1/TGF-β1/CD44s/STAT3 signaling between mesothelial cells and GC cells induces EMT and stemness phenotypes, offering potential as a therapeutic target for PM of GC.
MeSH term(s)	Humans ; Cell Line, Tumor ; Cell Movement ; Early Growth Response Protein 1/genetics ; Early Growth Response Protein 1/metabolism ; Epithelial-Mesenchymal Transition/physiology ; Hyaluronan Receptors/genetics ; Hyaluronan Receptors/metabolism ; Peritoneal Neoplasms ; Peritoneum/pathology ; Signal Transduction/genetics ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; Stomach Neoplasms/metabolism ; Transforming Growth Factor beta1/metabolism ; Tumor Microenvironment/genetics ; Animals
Chemical Substances	CD44 protein, human ; Early Growth Response Protein 1 ; EGR1 protein, human ; Hyaluronan Receptors ; STAT3 protein, human ; STAT3 Transcription Factor ; Transforming Growth Factor beta1 ; TGFB1 protein, human
Language	English
Publishing date	2024-01-27
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2179208-2
ISSN	1449-2288 ; 1449-2288
ISSN (online)	1449-2288
ISSN	1449-2288
DOI	10.7150/ijbs.90598
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Article ; Online: VPS35 promotes cell proliferation via EGFR recycling and enhances EGFR inhibitors response in gastric cancerResearch in context

Junxian Yu / Haoran Feng / Qingqing Sang / Fangyuan Li / Mengdi Chen / Beiqin Yu / Zhuoqing Xu / Tao Pan / Xiongyan Wu / Junyi Hou / Zhenggang Zhu / Chao Yan / Liping Su / Jianfang Li / Bingya Liu

EBioMedicine, Vol 89, Iss , Pp 104451- (2023)

2023

Abstract: Summary: Background: Vacuolar protein sorting-associated protein 35 (VPS35) is a core component of the retromer complex which mediates intracellular protein transport. It is well known that dysfunctional VPS35 functions in the accumulation of pathogenic ... ...

Abstract	Summary: Background: Vacuolar protein sorting-associated protein 35 (VPS35) is a core component of the retromer complex which mediates intracellular protein transport. It is well known that dysfunctional VPS35 functions in the accumulation of pathogenic proteins. In our previous study, VPS35 was found to be a potential gene related to poor prognosis in gastric cancer. However, the biological functions of VPS35 in gastric cancer remain unclear. Methods: Cell viability assays were performed to examine whether VPS35 affected cell proliferation. Immunoprecipitation and biotin assays showed that VPS35 bound to epidermal growth factor receptor (EGFR) in the cytoplasm and recycled it to the cell surface. Patient-derived xenografts and organoids were used to evaluate the effect of VPS35 on the response of gastric cancer to EGFR inhibitors. Findings: VPS35 expression levels were upregulated in tumour tissues and correlated with local tumour invasion and poor survival in patients with gastric cancer. VPS35 promoted cell proliferation and increased tumour growth. Mechanistically, VPS35 selectively bound to endocytosed EGFR in early endosomes and recycled it back to the cell surface, leading to the downstream activation of the ERK1/2 pathway. We also found that high VPS35 expression levels increased the sensitivity of the xenograft and organoid models to EGFR inhibitors. Interpretation: VPS35 promotes cell proliferation by recycling EGFR to the cell surface, amplifying the network of receptor trafficking. VPS35 expression levels are positively correlated with gastric cancer sensitivity to EGFR inhibitors, which offers a potential method to stratify patients for EGFR inhibitor utilisation. Funding: National Natural Science Foundation of China.
Keywords	VPS35 ; Retromer ; EGFR ; Erlotinib ; Gastric cancer ; Medicine ; R ; Medicine (General) ; R5-920
Subject code	616
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cancer-associated fibroblasts impair the cytotoxic function of NK cells in gastric cancer by inducing ferroptosis via iron regulation

Lizhong Yao / Junyi Hou / Xiongyan Wu / Yifan Lu / Zhijian Jin / Zhenjia Yu / Beiqin Yu / Jianfang Li / Zhongyin Yang / Chen Li / Min Yan / Zhenggang Zhu / Bingya Liu / Chao Yan / Liping Su

Redox Biology, Vol 67, Iss , Pp 102923- (2023)

2023

Abstract: As the predominant immunosuppressive component within the tumor microenvironment (TME), cancer-associated fibroblasts (CAFs) inhibit Natural Killer cell (NK cell) activity to promote tumor progression and immune escape; however, the mechanisms of cross- ... ...

Abstract	As the predominant immunosuppressive component within the tumor microenvironment (TME), cancer-associated fibroblasts (CAFs) inhibit Natural Killer cell (NK cell) activity to promote tumor progression and immune escape; however, the mechanisms of cross-talk between CAFs and NK cells in gastric cancer (GC) remain poorly understood. In this study, we demonstrate that NK cell levels are inversely correlated with CAFs abundance in human GC. CAFs impair the anti-tumor capacity of NK cells by inducing ferroptosis, a cell death process characterized by the accumulation of iron-dependent lipid peroxides. CAFs induce ferroptosis in NK cells by promoting iron overload; conversely, decreased intracellular iron levels protect NK cells against CAF-induced ferroptosis. Mechanistically, CAFs increase the labile iron pool within NK cells via iron export into the TME, which is mediated by the upregulated expression of iron regulatory genes ferroportin1 and hephaestin in CAFs. Moreover, CAF-derived follistatin like protein 1(FSTL1) upregulates NCOA4 expression in NK cells via the DIP2A-P38 pathway, and NCOA4-mediated ferritinophagy is required for CAF-induced NK cell ferroptosis. In a human patient-derived organoid model, functional targeting of CAFs using a combination of deferoxamine and FSTL1-neutralizing antibody significantly alleviate CAF-induced NK cell ferroptosis and boost the cytotoxicity of NK cells against GC. This study demonstrates a novel mechanism of suppression of NK cell activity by CAFs in the TME and presents a potential therapeutic approach to augment the immune response against GC mediated by NK cells.
Keywords	Cancer-associated fibroblasts ; NK cells ; Iron regulation ; Ferroptosis ; Ferritinophagy ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2023-11-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cancer-associated fibroblasts impair the cytotoxic function of NK cells in gastric cancer by inducing ferroptosis via iron regulation.

Yao, Lizhong / Hou, Junyi / Wu, Xiongyan / Lu, Yifan / Jin, Zhijian / Yu, Zhenjia / Yu, Beiqin / Li, Jianfang / Yang, Zhongyin / Li, Chen / Yan, Min / Zhu, Zhenggang / Liu, Bingya / Yan, Chao / Su, Liping

Redox biology

2023 Volume 67, Page(s) 102923

Abstract	As the predominant immunosuppressive component within the tumor microenvironment (TME), cancer-associated fibroblasts (CAFs) inhibit Natural Killer cell (NK cell) activity to promote tumor progression and immune escape; however, the mechanisms of cross-talk between CAFs and NK cells in gastric cancer (GC) remain poorly understood. In this study, we demonstrate that NK cell levels are inversely correlated with CAFs abundance in human GC. CAFs impair the anti-tumor capacity of NK cells by inducing ferroptosis, a cell death process characterized by the accumulation of iron-dependent lipid peroxides. CAFs induce ferroptosis in NK cells by promoting iron overload; conversely, decreased intracellular iron levels protect NK cells against CAF-induced ferroptosis. Mechanistically, CAFs increase the labile iron pool within NK cells via iron export into the TME, which is mediated by the upregulated expression of iron regulatory genes ferroportin1 and hephaestin in CAFs. Moreover, CAF-derived follistatin like protein 1(FSTL1) upregulates NCOA4 expression in NK cells via the DIP2A-P38 pathway, and NCOA4-mediated ferritinophagy is required for CAF-induced NK cell ferroptosis. In a human patient-derived organoid model, functional targeting of CAFs using a combination of deferoxamine and FSTL1-neutralizing antibody significantly alleviate CAF-induced NK cell ferroptosis and boost the cytotoxicity of NK cells against GC. This study demonstrates a novel mechanism of suppression of NK cell activity by CAFs in the TME and presents a potential therapeutic approach to augment the immune response against GC mediated by NK cells.
MeSH term(s)	Humans ; Cancer-Associated Fibroblasts/metabolism ; Cancer-Associated Fibroblasts/pathology ; Follistatin-Related Proteins/metabolism ; Ferroptosis ; Stomach Neoplasms/metabolism ; Iron/metabolism ; Killer Cells, Natural/metabolism ; Killer Cells, Natural/pathology ; Antineoplastic Agents/pharmacology ; Tumor Microenvironment
Chemical Substances	Follistatin-Related Proteins ; Iron (E1UOL152H7) ; Antineoplastic Agents ; FSTL1 protein, human (158709-61-6)
Language	English
Publishing date	2023-10-06
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2023.102923
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Article ; Online: VPS35 promotes cell proliferation via EGFR recycling and enhances EGFR inhibitors response in gastric cancer.

Yu, Junxian / Feng, Haoran / Sang, Qingqing / Li, Fangyuan / Chen, Mengdi / Yu, Beiqin / Xu, Zhuoqing / Pan, Tao / Wu, Xiongyan / Hou, Junyi / Zhu, Zhenggang / Yan, Chao / Su, Liping / Li, Jianfang / Liu, Bingya

EBioMedicine

2023 Volume 89, Page(s) 104451

Abstract: Background: Vacuolar protein sorting-associated protein 35 (VPS35) is a core component of the retromer complex which mediates intracellular protein transport. It is well known that dysfunctional VPS35 functions in the accumulation of pathogenic proteins. ...

Abstract	Background: Vacuolar protein sorting-associated protein 35 (VPS35) is a core component of the retromer complex which mediates intracellular protein transport. It is well known that dysfunctional VPS35 functions in the accumulation of pathogenic proteins. In our previous study, VPS35 was found to be a potential gene related to poor prognosis in gastric cancer. However, the biological functions of VPS35 in gastric cancer remain unclear. Methods: Cell viability assays were performed to examine whether VPS35 affected cell proliferation. Immunoprecipitation and biotin assays showed that VPS35 bound to epidermal growth factor receptor (EGFR) in the cytoplasm and recycled it to the cell surface. Patient-derived xenografts and organoids were used to evaluate the effect of VPS35 on the response of gastric cancer to EGFR inhibitors. Findings: VPS35 expression levels were upregulated in tumour tissues and correlated with local tumour invasion and poor survival in patients with gastric cancer. VPS35 promoted cell proliferation and increased tumour growth. Mechanistically, VPS35 selectively bound to endocytosed EGFR in early endosomes and recycled it back to the cell surface, leading to the downstream activation of the ERK1/2 pathway. We also found that high VPS35 expression levels increased the sensitivity of the xenograft and organoid models to EGFR inhibitors. Interpretation: VPS35 promotes cell proliferation by recycling EGFR to the cell surface, amplifying the network of receptor trafficking. VPS35 expression levels are positively correlated with gastric cancer sensitivity to EGFR inhibitors, which offers a potential method to stratify patients for EGFR inhibitor utilisation. Funding: National Natural Science Foundation of China.
MeSH term(s)	Humans ; Carrier Proteins/metabolism ; Cell Proliferation ; ErbB Receptors/antagonists & inhibitors ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; Protein Transport/drug effects ; Protein Transport/genetics ; Stomach Neoplasms/genetics ; Vesicular Transport Proteins/genetics ; Vesicular Transport Proteins/metabolism
Chemical Substances	Carrier Proteins ; EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1) ; Vesicular Transport Proteins ; VPS35 protein, human
Language	English
Publishing date	2023-02-02
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2023.104451
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Article ; Online: Paracrine activin B-NF-κB signaling shapes an inflammatory tumor microenvironment in gastric cancer via fibroblast reprogramming.

Jin, Yangbing / Cai, Qu / Wang, Lingquan / Ji, Jun / Sun, Ying / Jiang, Jinling / Wang, Chao / Wu, Junwei / Zhang, Benyan / Zhao, Liqin / Qi, Feng / Yu, Beiqin / Zhang, Jun

Journal of experimental & clinical cancer research : CR

2023 Volume 42, Issue 1, Page(s) 269

Abstract: Background: Important roles of INHBB in various malignancies are increasingly identified. The underlying mechanisms in gastric cancer (GC) microenvironment are still greatly unexplored.: Methods: The clinical significance of INHBB and the correlation ...

Abstract	Background: Important roles of INHBB in various malignancies are increasingly identified. The underlying mechanisms in gastric cancer (GC) microenvironment are still greatly unexplored. Methods: The clinical significance of INHBB and the correlation between INHBB and p-p65 in GC were assessed through analyzing publicly available databases and human paraffin embedded GC tissues. The biological crosstalk of INHBB between GC cells and fibroblasts was explored both in vitro and in vivo. RNA-seq analyses were performed to determine the mechanisms which regulating fibroblasts reprogramming. Luciferase reporter assay and chromatin immunoprecipitation (CHIP) assay were used to verify the binding relationship of p65 and INHBB in GC cells. Results: Our study showed that INHBB level was significantly higher in GC, and that increased INHBB was associated with poor survival. INHBB positively regulates the proliferation, migration, and invasion of GC cells in vitro. Also, activin B promotes the occurrence of GC by reprogramming fibroblasts into cancer-associated fibroblasts (CAFs). The high expression of INHBB in GC cells activates the NF-κB pathway of normal gastric fibroblasts by secreting activin B, and promotes fibroblasts proliferation, migration, and invasion. In addition, activin B activates NF-κB pathway by controlling TRAF6 autoubiquitination to induce TAK1 phosphorylation in fibroblasts. Fibroblasts activated by activin B can induce the activation of p65 phosphorylation of GC cells by releasing pro-inflammatory factors IL-1β. p65 can directly bind to the INHBB promoter and increase the INHBB transcription of GC cells, thus establishing a positive regulatory feedback loop to promote the progression of GC. Conclusions: GC cells p65/INHBB/activin B and fibroblasts p65/IL-1β signal loop led to the formation of a whole tumor-promoting inflammatory microenvironment, which might be a promising therapeutic target for GC.
MeSH term(s)	Humans ; Cell Line, Tumor ; Fibroblasts/metabolism ; NF-kappa B/metabolism ; Stomach Neoplasms/pathology ; Tumor Microenvironment/physiology ; Activins/metabolism
Chemical Substances	activin B ; NF-kappa B ; INHBB protein, human ; Activins (104625-48-1)
Language	English
Publishing date	2023-10-19
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/s13046-023-02861-4
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Zs.A 2065: Show issues

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Article ; Online: Androgen receptor promotes cell stemness via interacting with co-factor YAP1 in gastric cancer.

Hou, Junyi / Pan, Tao / Li, Fangyuan / Sang, Qingqing / Wu, Xiongyan / Li, Jianfang / Yu, Beiqin / Zang, Mingde / Zhu, Zheng-Gang / Su, Liping / Liu, Bingya

Biochemical pharmacology

2023 Volume 217, Page(s) 115849

Abstract: Cancer stem cells (CSCs) have been proposed to explain tumor relapse and chemoresistance in various types of cancers, and androgen receptor (AR) has been emerged as a potential regulator of stemness in cancers. However, the underlying mechanism of AR- ... ...

Abstract	Cancer stem cells (CSCs) have been proposed to explain tumor relapse and chemoresistance in various types of cancers, and androgen receptor (AR) has been emerged as a potential regulator of stemness in cancers. However, the underlying mechanism of AR-regulated CSCs properties and chemoresistance in gastric cancer (GC) remains unknown. Here, we shown that AR is upregulated in GC tissues and correlates with poor survival rate and CSCs phenotypes of GC patients. According to our experimental data, overexpression of AR upregulated the expression of CSCs markers and this was consistent with the result concluded from data analysis that the expression of AR was positively correlated with CD44 in GC patients. In addition, AR overexpression obviously enhanced the tumor sphere formation ability and chemoresistance of GC cells in vitro. Whereas these effects were attenuated by inhibition of AR. These results were further validated in vivo that MGC-803 cells overexpressing AR had stronger properties to initiate gastric tumorigenesis than the control cells, and inhibition of AR increased the chemosensitivity of GC cells. Mechanically, AR upregulated CD44 expression by directly binding to its promoter region and Yes-associated protein 1 (YAP1) served as the co-factor of AR, which was demonstrated by the fact that the promoting effects of AR on GC cells stemness were partially counteracted by YAP1 knockdown. Thus, this study revealed that AR facilitates CSCs properties and chemoresistance of GC cells via forming complex with YAP1and indicates a potential therapeutic approach to GC patients.
MeSH term(s)	Humans ; Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Neoplasm Recurrence, Local/genetics ; Neoplasm Recurrence, Local/metabolism ; Neoplasm Recurrence, Local/pathology ; Neoplastic Stem Cells/pathology ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism ; Stomach Neoplasms/drug therapy ; Stomach Neoplasms/genetics ; Stomach Neoplasms/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; YAP-Signaling Proteins/genetics ; YAP-Signaling Proteins/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Receptors, Androgen ; Transcription Factors ; YAP-Signaling Proteins
Language	English
Publishing date	2023-10-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2023.115849
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