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Article ; Online: Simultaneous submission of seven CTSA proposals: UM1, K12, R25, T32-predoctoral, T32-postdoctoral, and RC2: strategies, evaluation, and lessons learned.

Lema, Carolina / Cheng, Kwai Wa / Anderson, Delanderia M / Miller, Charles C / Karp, Daniel D / McPherson, David D / Kolar, Satya Sree N

Journal of clinical and translational science

2024 Volume 8, Issue 1, Page(s) e33

Abstract: Translation is the process of turning observations in the research laboratory, clinic, and community into interventions that improve people's health. The Clinical and Translational Science Awards (CTSA) program is a National Center for Advancing ... ...

Abstract	Translation is the process of turning observations in the research laboratory, clinic, and community into interventions that improve people's health. The Clinical and Translational Science Awards (CTSA) program is a National Center for Advancing Translational Sciences (NCATS) initiative to advance translational science and research. Currently, 64 "CTSA hubs" exist across the nation. Since 2006, the Houston-based Center for Clinical Translational Sciences (CCTS) has assembled a well-integrated, high-impact hub in Texas that includes six partner institutions within the state, encompassing ∼23,000 sq. miles and over 16 million residents. To achieve the NCATS goal of "more treatments for all people more quickly," the CCTS promotes diversity and inclusion by integrating underrepresented populations into clinical studies, workforce training, and career development. In May 2023, we submitted the UM1 application and six "companion" proposals: K12, R25, T32-Predoctoral, T32-Postdoctoral, and RC2 (two applications). In October 2023, we received priority scores for the UM1 (22), K12 (25), T32-Predoctoral (20), and T32-Postdoctoral (23), which historically fall within the NCATS funding range. This report describes the grant preparation and submission approach, coupled with data from an internal survey designed to assimilate feedback from principal investigators, writers, reviewers, and administrative specialists. Herein, we share the challenges faced, the approaches developed, and the lessons learned.
Language	English
Publishing date	2024-01-25
Publishing country	England
Document type	Journal Article
ISSN	2059-8661
ISSN (online)	2059-8661
DOI	10.1017/cts.2024.14
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Article: Ras-superfamily GTP-ases in ovarian cancer.

Cheng, Kwai Wa / Agarwal, Roshan / Mills, Gordon B

Cancer treatment and research

2009 Volume 149, Page(s) 229–240

MeSH term(s)	Cell Transformation, Neoplastic ; Female ; Genes, ras ; Humans ; Mutation ; Neoplasm Proteins/physiology ; Ovarian Neoplasms/enzymology ; Phosphorylation ; Protein Processing, Post-Translational ; rab GTP-Binding Proteins/physiology ; ras Proteins/physiology ; rho GTP-Binding Proteins/physiology
Chemical Substances	Neoplasm Proteins ; rab GTP-Binding Proteins (EC 3.6.5.2) ; ras Proteins (EC 3.6.5.2) ; rho GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2009-10-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	0927-3042
ISSN	0927-3042
DOI	10.1007/978-0-387-98094-2_11
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Article ; Online: The emerging role of the RAB25 small GTPase in cancer.

Agarwal, Roshan / Jurisica, Igor / Mills, Gordon B / Cheng, Kwai Wa

Traffic (Copenhagen, Denmark)

2009 Volume 10, Issue 11, Page(s) 1561–1568

Abstract: RAB25, a member of the rat sarcoma (RAS) family of small GTPase, has been implicated in the pathophysiology of ovarian, breast and other cancers. Its role in endosomal transport and recycling of cell-surface receptors and signaling proteins presents a ... ...

Abstract	RAB25, a member of the rat sarcoma (RAS) family of small GTPase, has been implicated in the pathophysiology of ovarian, breast and other cancers. Its role in endosomal transport and recycling of cell-surface receptors and signaling proteins presents a novel paradigm for the disruption of cellular pathways and promotion of tumor development and aggressiveness. Variations in structure and post-translational modifications control the localization of RAS superfamily proteins to specific subcellular compartments and recruitment of downstream effectors, allowing these small GTPases to function as sophisticated modulators of a complex and diverse range of cellular processes. Here, we review the link between RAB25 and tumor development and current knowledge regarding its possible roles in cancer.
MeSH term(s)	Animals ; Female ; Humans ; Mammary Neoplasms, Experimental/genetics ; Mammary Neoplasms, Experimental/pathology ; Models, Biological ; Monomeric GTP-Binding Proteins/genetics ; Monomeric GTP-Binding Proteins/metabolism ; Neoplasms/genetics ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Rats ; rab GTP-Binding Proteins/physiology ; ras Proteins/physiology
Chemical Substances	Monomeric GTP-Binding Proteins (EC 3.6.5.2) ; rab GTP-Binding Proteins (EC 3.6.5.2) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2009-07-27
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1483852-7
ISSN	1600-0854 ; 1398-9219
ISSN (online)	1600-0854
ISSN	1398-9219
DOI	10.1111/j.1600-0854.2009.00969.x
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Article: Assay of Rab25 function in ovarian and breast cancers.

Cheng, Kwai Wa / Lu, Yiling / Mills, Gordon B

Methods in enzymology

2005 Volume 403, Page(s) 202–215

Abstract: There is a multitude of critical steps during the pathogenesis of cancer that allow cells to acquire the ability to escape from normal controls on cell growth, to avoid programmed cell death, and to become malignant. Here, we describe a molecular ... ...

Abstract	There is a multitude of critical steps during the pathogenesis of cancer that allow cells to acquire the ability to escape from normal controls on cell growth, to avoid programmed cell death, and to become malignant. Here, we describe a molecular approach that can be broadly applied to identify drivers of genomic aberrations in cancer development. In the process, areas of genomic aberrations and genes that are dysregulated by genomic amplification are identified by array comparative genomic hybridization (CGH) and transcription profiling, respectively, with major emphasis on coordinating amplification at the CGH and RNA level and on correlation with patient's outcomes. Once candidate genes are identified, we perform functional genomics by manipulating levels in normal and tumor cells using RNAi or transfection, and assessing a battery of cellular functions including proliferation, anti-apoptosis, loss of contact inhibition, changes in cell signaling or transcriptional profiles, anchorage-independent growth, and in vivo tumor growth. We have successfully used this approach to identify the RAB25 gene that has been implicated in the progression and aggressiveness of ovarian and breast cancers.
MeSH term(s)	Apoptosis ; Base Sequence ; Breast Neoplasms/pathology ; Breast Neoplasms/physiopathology ; DNA Primers ; Female ; Humans ; Ovarian Neoplasms/pathology ; Ovarian Neoplasms/physiopathology ; Reverse Transcriptase Polymerase Chain Reaction ; rab GTP-Binding Proteins/physiology
Chemical Substances	DNA Primers ; Rab25 protein, human ; rab GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2005
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	0076-6879
ISSN	0076-6879
DOI	10.1016/S0076-6879(05)03017-X
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Article: The Emerging Role of the RAB25 Small GTPase in Cancer

Agarwal, Roshan / Jurisica, Igor / Mills, Gordon B / Cheng, Kwai Wa

Traffic. 2009 Nov., v. 10, no. 11

2009

Abstract	RAB25, a member of the rat sarcoma (RAS) family of small GTPase, has been implicated in the pathophysiology of ovarian, breast and other cancers. Its role in endosomal transport and recycling of cell-surface receptors and signaling proteins presents a novel paradigm for the disruption of cellular pathways and promotion of tumor development and aggressiveness. Variations in structure and post-translational modifications control the localization of RAS superfamily proteins to specific subcellular compartments and recruitment of downstream effectors, allowing these small GTPases to function as sophisticated modulators of a complex and diverse range of cellular processes. Here, we review the link between RAB25 and tumor development and current knowledge regarding its possible roles in cancer.
Keywords	neoplasms ; endocytosis
Language	English
Dates of publication	2009-11
Size	p. 1561-1568.
Publisher	Blackwell Publishing Ltd
Publishing place	Oxford, UK
Document type	Article
ZDB-ID	1483852-7
ISSN	1600-0854 ; 1398-9219
ISSN (online)	1600-0854
ISSN	1398-9219
DOI	10.1111/j.1600-0854.2009.00969.x
Database	NAL-Catalogue (AGRICOLA)

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Article: Analysis of molecular aberrations in ovarian cancer allows novel target identification.

Cheng, Kwai Wa / Lahad, John P / Mills, Gordon B

Journal of obstetrics and gynaecology Canada : JOGC = Journal d'obstetrique et gynecologie du Canada : JOGC

2004 Volume 26, Issue 5, Page(s) 461–474

Abstract: The completion of the Human Genome Project and recent advances in functional genomic, proteomic, and high-throughput screening methodologies have provided powerful tools for determining the mechanisms of human diseases, including complex polygenic ... ...

Abstract	The completion of the Human Genome Project and recent advances in functional genomic, proteomic, and high-throughput screening methodologies have provided powerful tools for determining the mechanisms of human diseases, including complex polygenic diseases such as ovarian cancer. These developments may eventually lead to individualized molecular medicine, which is the treatment of patients based on the underlying genetic defects in their tumours and their own genetic makeup. A plethora of novel therapeutic agents that act on specific molecular targets defined by cancer genetics are under development. There is thus a great deal of interest in determining how specific genes and proteins function in cancers, in order to further the understanding of cancer initiation and progression; to aid in identifying biomarkers, therapeutic targets, and determinants of drug responsiveness; and to progress the development of novel antitumour agents.
MeSH term(s)	Antineoplastic Agents ; DNA Mutational Analysis ; Drug Design ; Female ; Gene Expression ; Humans ; In Situ Hybridization, Fluorescence ; Mutation ; Nucleic Acid Hybridization ; Oligonucleotide Array Sequence Analysis ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/epidemiology ; Ovarian Neoplasms/genetics ; Polymorphism, Single-Stranded Conformational ; Proteomics
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2004-05-06
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2171082-X
ISSN	1701-2163
ISSN	1701-2163
DOI	10.1016/s1701-2163(16)30657-0
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Zs.A 6445: Show issues

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Article: Human chorionic gonadotropin-activated cAMP pathway regulates human placental GnRH receptor gene transcription in choriocarcinoma JEG-3 cells.

Cheng, Kwai Wa / Leung, Peter C K

The Journal of clinical endocrinology and metabolism

2002 Volume 87, Issue 7, Page(s) 3291–3299

Abstract: A dose- and time-dependent increase in the human GnRH receptor (GnRHR) promoter activity after forskolin treatment was observed after transient transfection of human placental choriocarcinoma JEG-3 cells with a 2297-bp human GnRHR promoter-luciferase ... ...

Abstract	A dose- and time-dependent increase in the human GnRH receptor (GnRHR) promoter activity after forskolin treatment was observed after transient transfection of human placental choriocarcinoma JEG-3 cells with a 2297-bp human GnRHR promoter-luciferase construct (p2300-LucF). This stimulatory effect was mimicked by administrating of cholera toxin, cAMP analog, or human chorionic gonadotropin. A specific adenylate cyclase inhibitor or protein kinase A inhibitor pretreatment reversed the forskolin- and human chorionic gonadotropin-induced increase in the human GnRHR promoter activity. Progressive 5' deletion assays identified a 412-bp fragment (-577 to -167) in the human GnRHR 5'-flanking region that is essential in maintaining the basal responsiveness to cAMP. Mutagenesis, coupled with functional studies, has identified two putative activating protein-1 (AP-1)/cAMP-responsive element (CRE) binding protein binding sites, namely human GnRHR (hGR)-AP/CRE-1 and hGR-AP/CRE-2, mediating the cAMP-stimulatory effect. Mutation of the putative hGR-AP/CRE-1 and hGR-AP/CRE-2 resulted in 32% and 35% decreases in the forskolin-induced stimulation, respectively. The binding of CRE binding protein to these motifs was confirmed by gel mobility shift assay and antibody supershift assay.
MeSH term(s)	8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Adenylyl Cyclases/physiology ; Base Sequence/genetics ; Binding Sites ; Chorionic Gonadotropin/pharmacology ; Colforsin/pharmacology ; Cyclic AMP/physiology ; Cyclic AMP Response Element-Binding Protein/genetics ; Cyclic AMP Response Element-Binding Protein/metabolism ; Cyclic AMP-Dependent Protein Kinases/physiology ; Humans ; Placenta/metabolism ; Promoter Regions, Genetic/drug effects ; Promoter Regions, Genetic/physiology ; Receptors, LHRH/genetics ; Transcription Factor AP-1/metabolism ; Transcription, Genetic/physiology ; Tumor Cells, Cultured ; Up-Regulation/physiology
Chemical Substances	Chorionic Gonadotropin ; Cyclic AMP Response Element-Binding Protein ; Receptors, LHRH ; Transcription Factor AP-1 ; Colforsin (1F7A44V6OU) ; 8-Bromo Cyclic Adenosine Monophosphate (23583-48-4) ; Cyclic AMP (E0399OZS9N) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; Adenylyl Cyclases (EC 4.6.1.1)
Language	English
Publishing date	2002-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/jcem.87.7.8650
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Article ; Online: Knockdown of RAB25 promotes autophagy and inhibits cell growth in ovarian cancer cells.

Liu, Yingtao / Tao, Xiang / Jia, Luoqi / Cheng, Kwai Wa / Lu, Yiling / Yu, Yinhua / Feng, Youji

Molecular medicine reports

2012 Volume 6, Issue 5, Page(s) 1006–1012

Abstract: RAB25 belongs to the Rab family of small GTPases and is implicated in the development of various types of human cancer. To evaluate the role of RAB25 in ovarian cancer, RAB25 was knocked down by siRNA in HEY and ES‑2 human ovarian ...

Abstract	RAB25 belongs to the Rab family of small GTPases and is implicated in the development of various types of human cancer. To evaluate the role of RAB25 in ovarian cancer, RAB25 was knocked down by siRNA in HEY and ES‑2 human ovarian cancer cells. Autophagy, cell growth and cell apoptosis were evaluated. The results showed that knockdown of RAB25 increased acidic vesicle organelles and GFP-microtubule-associated protein 1 light chain 3 punctate fluorescence in ovarian cancer cells. Autophagy that promoted by knockdown of RAB25 was not observed in cells where the ERK1/2 signaling pathway had been inhibited by U0126. Knockdown of RAB25 reduced cell cycle progression and cell growth. Apoptosis of ovarian cancer cells could be induced by knockdown of RAB25. These results support the tumorigenic role of RAB25 in ovarian cancer cells.
MeSH term(s)	Apoptosis ; Autophagy ; Butadienes/pharmacology ; Cell Line, Tumor ; Cell Proliferation ; Female ; Humans ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Nitriles/pharmacology ; Ovarian Neoplasms/metabolism ; Ovarian Neoplasms/pathology ; RNA Interference ; RNA, Small Interfering/metabolism ; Signal Transduction/drug effects ; rab GTP-Binding Proteins/antagonists & inhibitors ; rab GTP-Binding Proteins/genetics ; rab GTP-Binding Proteins/metabolism
Chemical Substances	Butadienes ; Nitriles ; RNA, Small Interfering ; Rab25 protein, human ; U 0126 ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; rab GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2012-08-28
Publishing country	Greece
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2469505-1
ISSN	1791-3004 ; 1791-2997
ISSN (online)	1791-3004
ISSN	1791-2997
DOI	10.3892/mmr.2012.1052
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Article ; Online: Rab25 increases cellular ATP and glycogen stores protecting cancer cells from bioenergetic stress.

Cheng, Kwai Wa / Agarwal, Roshan / Mitra, Shreya / Lee, Ju-Seog / Carey, Mark / Gray, Joe W / Mills, Gordon B

EMBO molecular medicine

2012 Volume 4, Issue 2, Page(s) 125–141

Abstract: Cancer cells are metabolically stressed during tumour progression due to limited tumour vascularity and resultant nutrient, growth factor and oxygen deficiency that can induce cell death and inhibit tumour growth. We demonstrate that Rab25, a small ... ...

Abstract	Cancer cells are metabolically stressed during tumour progression due to limited tumour vascularity and resultant nutrient, growth factor and oxygen deficiency that can induce cell death and inhibit tumour growth. We demonstrate that Rab25, a small GTPase involved in endosomal recycling, that is genomically amplified in multiple tumour lineages, is a key regulator of cellular bioenergetics and autophagy. RAB25 enhanced survival during nutrient stress by preventing apoptosis and autophagy via binding and activating AKT leading to increased glucose uptake and improved cellular bioenergetics. Unexpectedly, Rab25 induced the accumulation of glycogen in epithelial cancer cells, a process not previously identified. Strikingly, an increase in basal ATP levels combined with AKT-dependent increases in glucose uptake and glycogen storage allowed maintenance of ATP levels during bioenergetic stress. The clinical relevance of these findings was validated by the ability of a Rab25-dependent expression profile enriched for bioenergetics targets to identify patients with a poor prognosis. Thus, Rab25 is an unexpected regulator of cellular bioenergetics implicated as a useful biomarker and potential therapeutic target.
MeSH term(s)	Adenosine Triphosphate/metabolism ; Apoptosis ; Autophagy ; Cell Death/physiology ; Energy Metabolism ; Glycogen/metabolism ; Humans ; Neoplasms/metabolism ; Tumor Cells, Cultured ; rab GTP-Binding Proteins/genetics ; rab GTP-Binding Proteins/metabolism
Chemical Substances	Rab25 protein, human ; Adenosine Triphosphate (8L70Q75FXE) ; Glycogen (9005-79-2) ; rab GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2012-01-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.1002/emmm.201100193
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Article ; Online: FSH inhibits ovarian cancer cell apoptosis by up-regulating survivin and down-regulating PDCD6 and DR5.

Huang, Yan / Jin, Hongyan / Liu, Yingtao / Zhou, Jiayi / Ding, Jingxin / Cheng, Kwai Wa / Yu, Yinhua / Feng, Youji

Endocrine-related cancer

2011 Volume 18, Issue 1, Page(s) 13–26

Abstract: Ovarian epithelial cancer is the leading cause of death among gynecological malignancies. FSH may increase the risk of ovarian malignancy and play an important role in ovarian carcinogenesis. Our previous studies showed that FSH increases the expression ... ...

Abstract	Ovarian epithelial cancer is the leading cause of death among gynecological malignancies. FSH may increase the risk of ovarian malignancy and play an important role in ovarian carcinogenesis. Our previous studies showed that FSH increases the expression of VEGF through survivin. In this study, the function and mechanism of FSH in ovarian cancer were further explored. We found that FSH promoted proliferation and prevented apoptosis of ovarian cancer cells by activating survivin through the SAPK/JNK and PI3K/AKT pathways. FSH also down-regulated the expression of programmed cell death gene 6 (PDCD6) and death receptor 5 (DR5), two molecules required for induction of apoptosis. RNA interference was applied to knock down survivin and PDCD6 expression, and we found that the blockage of survivin reversed the effects of FSH on apoptosis and proliferation, whereas knock down of PDCD6 enhanced these effects. The expression of DR5, cyclin D1, and cyclin E correlated with survivin expression, but PDCD6 did not. Using immunohistochemical staining, we further showed that ovarian serous cystadenocarcinoma samples had higher expression of survivin than did benign ovarian cystadenoma and borderline cystadenoma samples (P<0.01). Furthermore, survivin expression in the ovarian serous cystadenocarcinoma specimens was correlated with disease stage (P<0.05). Our results suggest that FSH promotes ovarian cancer development by regulating the expression of survivin, PDCD6, and DR5. Greater understanding of the molecular mechanisms of FSH in ovarian epithelial carcinogenesis and development will ultimately help in the development of a novel targeted therapy for ovarian cancer.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Apoptosis Regulatory Proteins/analysis ; Apoptosis Regulatory Proteins/antagonists & inhibitors ; Calcium-Binding Proteins/analysis ; Calcium-Binding Proteins/antagonists & inhibitors ; Cell Cycle/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cyclin D1/analysis ; Cyclin E/analysis ; Female ; Follicle Stimulating Hormone/pharmacology ; Humans ; Inhibitor of Apoptosis Proteins ; JNK Mitogen-Activated Protein Kinases/physiology ; Mice ; Mice, Inbred BALB C ; Microtubule-Associated Proteins/analysis ; Ovarian Neoplasms/chemistry ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/pathology ; Phosphatidylinositol 3-Kinases/physiology ; Receptors, TNF-Related Apoptosis-Inducing Ligand/analysis ; Receptors, TNF-Related Apoptosis-Inducing Ligand/antagonists & inhibitors ; Signal Transduction/drug effects
Chemical Substances	Apoptosis Regulatory Proteins ; BIRC5 protein, human ; Calcium-Binding Proteins ; Cyclin E ; Inhibitor of Apoptosis Proteins ; Microtubule-Associated Proteins ; PDCD6 protein, human ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Cyclin D1 (136601-57-5) ; Follicle Stimulating Hormone (9002-68-0) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2011-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1218450-0
ISSN	1479-6821 ; 1351-0088
ISSN (online)	1479-6821
ISSN	1351-0088
DOI	10.1677/ERC-09-0308
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