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1. Full Text PI3K/mTOR dual inhibitor NVP-BEZ235 decreases Mcl-1 expression and sensitizes ovarian carcinoma cells to Bcl-xL -targeting strategies, provided that Bim expression is induced
by Jebahi, Abdelghani and Villedieu, Marie and Pétigny-Lechartier, Cécile and Brotin, Emilie and Louis, Marie-Hélène and Abeilard, Edwige and Giffard, Florence and Guercio, Marika and Briand, Mélanie and Gauduchon, Pascal and Lheureux, Stéphanie and Poulain, Laurent
Cancer Letters, ISSN 0304-3835, 2014, Volume 348, Issue 1, pp. 38 - 49
Abstract We previously showed that Bcl-xL and Mcl-1 cooperatively protect platinum-resistant ovarian cancer cells from apoptosis. Here we assessed the... 
Hematology, Oncology and Palliative Medicine | NVP-BEZ235 | ABT-737 | Mcl-1 | ERK1/2 | Bim | Ovarian cancer | TOR Serine-Threonine Kinases - metabolism | Phosphatidylinositol 3-Kinase - antagonists & inhibitors | Humans | Gene Expression Regulation, Neoplastic | Myeloid Cell Leukemia Sequence 1 Protein - metabolism | Ovarian Neoplasms - pathology | bcl-X Protein - genetics | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Extracellular Signal-Regulated MAP Kinases - metabolism | Quinolines - pharmacology | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Dose-Response Relationship, Drug | Ovarian Neoplasms - genetics | TOR Serine-Threonine Kinases - antagonists & inhibitors | Proto-Oncogene Proteins c-bcl-2 - metabolism | Transfection | Bcl-2-Like Protein 11 | Biphenyl Compounds - pharmacology | Nitrophenols - pharmacology | RNA Interference | Time Factors | bcl-X Protein - antagonists & inhibitors | Apoptosis Regulatory Proteins - genetics | Female | Membrane Proteins - metabolism | Phosphatidylinositol 3-Kinase - metabolism | Proto-Oncogene Proteins - metabolism | Myeloid Cell Leukemia Sequence 1 Protein - antagonists & inhibitors | Membrane Proteins - genetics | Proto-Oncogene Proteins - genetics | Imidazoles - pharmacology | Sulfonamides - pharmacology | Piperazines - pharmacology | Ovarian Neoplasms - enzymology | Apoptosis Regulatory Proteins - metabolism | Signal Transduction - drug effects | Cell Line, Tumor | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | bcl-X Protein - metabolism | Chemotherapy | Kinases | Apoptosis
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2. Full Text MicroRNA-125b promotes apoptosis by regulating the expression of Mcl-1, Bcl-w and IL-6R
by Gong, J and Zhang, J.-P and Li, B and Zeng, C and You, K and Chen, M.-X and Yuan, Y and Zhuang, S.-M
Oncogene, ISSN 0950-9232, 06/2013, Volume 32, Issue 25, pp. 3071 - 3079
The microRNA miR-125b is multi-faceted, with the ability to function as a tumor suppressor or an oncogene, depending on the cellular context. To date, the... 
IL-6R | Mcl-1 | apoptosis | miR-125b | Bcl-w | hepatocellular carcinoma | TARGET | CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | PROLIFERATION | CELL BIOLOGY | HEPATOCELLULAR-CARCINOMA | GENE | ONCOLOGY | DEREGULATION | GROWTH | GENETICS & HEREDITY | SUPPRESSES | Interleukin-6 - antagonists & inhibitors | Humans | Lung Neoplasms - metabolism | Caspase 3 - metabolism | Apoptosis - genetics | MicroRNAs - metabolism | Apoptosis Regulatory Proteins - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | Transfection | Myeloid Cell Leukemia Sequence 1 Protein | Liver Neoplasms - metabolism | Cell Line, Tumor | MicroRNAs - genetics | STAT3 Transcription Factor - antagonists & inhibitors | bcl-X Protein - metabolism | Interleukin-6 - metabolism | Colorectal Neoplasms - metabolism | STAT3 Transcription Factor - metabolism | Carcinoma, Hepatocellular - metabolism | Receptors, Interleukin-6 - metabolism | Care and treatment | MicroRNA | Colorectal cancer | Physiological aspects | Development and progression | Genetic aspects | Research | Apoptosis | Liver cancer | Signal transduction | Gene expression | Ribonucleic acid--RNA
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3. Full Text The lncRNA MALAT1 functions as a competing endogenous RNA to regulate MCL‐1 expression by sponging miR‐363‐3p in gallbladder cancer
by Wang, Shou‐Hua and Zhang, Wen‐Jie and Wu, Xiao‐Cai and Weng, Ming‐Zhe and Zhang, Ming‐Di and Cai, Qiang and Zhou, Di and Wang, Jian‐Dong and Quan, Zhi‐Wei
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 12/2016, Volume 20, Issue 12, pp. 2299 - 2308
Gallbladder carcinoma (GBC) is an aggressive neoplasm, and the treatment options for advanced GBC are limited. Recently, long non‐coding RNAs (lncRNAs) have... 
gallbladder cancer | MALAT1 | competing endogenous RNA | miR‐363‐3p | MCL‐1 | MCL-1 | miR-363-3p | MEDICINE, RESEARCH & EXPERIMENTAL | PREDICTS | APOPTOSIS | METASTASIS | DOWN-REGULATION | CELL BIOLOGY | MYELOID CELL LEUKEMIA-1 | LONG NONCODING RNA | POOR-PROGNOSIS | PROMOTES | CARCINOMA | Cell Cycle - genetics | Cell Proliferation - genetics | Gene Expression Regulation, Neoplastic | Myeloid Cell Leukemia Sequence 1 Protein - metabolism | Gallbladder Neoplasms - genetics | Apoptosis - genetics | Male | MicroRNAs - metabolism | RNA, Long Noncoding - genetics | Down-Regulation - genetics | Myeloid Cell Leukemia Sequence 1 Protein - genetics | Gene Knockdown Techniques | Animals | Mice, Nude | Base Sequence | Cell Line, Tumor | Tumor Burden - genetics | Gallbladder Neoplasms - pathology | MicroRNAs - genetics | RNA, Long Noncoding - metabolism | Genetic research | RNA | Analysis | Leukemia | Gallbladder cancer | Gallbladder | Gene expression | Ribonucleic acid--RNA | Stomach cancer | Original
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4. Full Text MMSET I acts as an oncoprotein and regulates GLO1 expression in t(4;14) multiple myeloma cells
by Xie, Zhigang and Chooi, Jing Yuan and Toh, Sabrina Hui Min and Yang, Dongxiao and Basri, Nurhidayah Binte and Ho, Ying Swan and Chng, Wee Joo
Leukemia, ISSN 0887-6924, 03/2019, Volume 33, Issue 3, pp. 739 - 748
Multiple myeloma (MM) is characterized by recurrent chromosomal translocations. T(4;14) MM overexpresses multiple myeloma SET domain-containing protein... 
CANCER-CELLS | T(4/14)(P16,Q32) | ADHESION | GENE | ONCOLOGY | TRANSLOCATIONS | POOR-PROGNOSIS | CD44 VARIANT 6 | T(4/14) MYELOMA | HEMATOLOGY | FGFR3 | HISTONE METHYLTRANSFERASE | Oncogene Proteins - genetics | Histone-Lysine N-Methyltransferase - genetics | Humans | Carcinogenesis - genetics | Lactoylglutathione Lyase - genetics | Cell Survival - genetics | Repressor Proteins - genetics | Apoptosis - genetics | Chromosomes, Human, Pair 4 - genetics | Glycolysis - genetics | Cell Line, Tumor | Chromatin Immunoprecipitation - methods | Chromosomes, Human, Pair 14 - genetics | Gene Expression Regulation, Neoplastic - genetics | Multiple Myeloma - genetics | Protein Isoforms - genetics | Translocation, Genetic - genetics | Care and treatment | Genetic aspects | Research | Gene expression | Chromosomes | Multiple myeloma | Chromatin | Immunoprecipitation | Cell survival | Transcription | Therapeutic applications | Mcl-1 protein | Mutants | Proteins | Chromosome translocations | Isoforms | Glycolysis | Tumorigenesis | Lactoylglutathione lyase | Protein transport | Apoptosis
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5. Full Text Activation of TWIST1 by COL11A1 promotes chemoresistance and inhibits apoptosis in ovarian cancer cells by modulating NF‐κB‐mediated IKKβ expression
by Wu, Yi‐Hui and Huang, Yu‐Fang and Chang, Tzu‐Hao and Chou, Cheng‐Yang
International Journal of Cancer, ISSN 0020-7136, 12/2017, Volume 141, Issue 11, pp. 2305 - 2317
We have shown that collagen type XI alpha 1 (COL11A1) promotes ovarian cancer progression and is associated with chemoresistance to cisplatin and paclitaxel in... 
TWIST1 | chemoresistance | anti‐apoptosis | epithelial ovarian carcinoma | collagen type XI alpha 1 | anti-apoptosis | CARCINOMA-CELLS | ANTICANCER DRUG CISPLATIN | COPPER TRANSPORTER | SENSITIVITY | CHEMOTHERAPY | EPITHELIAL-MESENCHYMAL TRANSITION | OVEREXPRESSION | ONCOLOGY | PATHWAY | RESISTANCE | UP-REGULATION | Mutagenesis, Site-Directed | Humans | Kaplan-Meier Estimate | Ovarian Neoplasms - pathology | NF-kappa B - metabolism | Nuclear Proteins - metabolism | Ovarian Neoplasms - mortality | Collagen Type XI - metabolism | Blotting, Western | Gene Knockdown Techniques | Disease-Free Survival | Chromatin Immunoprecipitation | I-kappa B Kinase - metabolism | Polymerase Chain Reaction | Female | Ovarian Neoplasms - metabolism | Apoptosis - physiology | Twist-Related Protein 1 - metabolism | Drug Resistance, Neoplasm - physiology | Gene Expression Regulation, Neoplastic - physiology | Phosphorylation | Ovarian carcinoma | Chemoresistance | Activation | Kinases | IKK protein | Ovarian cancer | Transcription activation | Paclitaxel | Helix-loop-helix proteins | Binding | NF-κB protein | siRNA | Sp1 protein | Gene expression | Survival | Patients | Cisplatin | Mcl-1 protein | Chemotherapy | Ribonucleic acids | Medical prognosis | Collagen | Tumors | Cancer | Apoptosis | Index Medicus
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6. Full Text The tyrosine kinase Syk regulates the survival of chronic lymphocytic leukemia B cells through PKC and proteasome-dependent regulation of Mcl-1 expression
by Baudot, A.D and Jeandel, P.Y and Mouska, X and Maurer, U and Tartare-Deckert, S and Raynaud, S.D and Cassuto, J.P and Ticchioni, M and Deckert, M
Oncogene, ISSN 0950-9232, 09/2009, Volume 28, Issue 37, pp. 3261 - 3273
B-cell chronic lymphocytic leukemia (B-CLL) is characterized by accumulation of mature monoclonal CD5+ B cells. The disease results mainly from a failure of... 
Mcl-1 | Syk | Survival | PKCdelta | B-CLL | Proteasome | Cell receptors | Chronic lymphocytic leukemia | Physiological aspects | Protein tyrosine kinase | Genetic aspects | Research | Genetic regulation | Signal transduction | Genetics | Cellular biology | Leukemia | Apoptosis
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7. Full Text The let-7 family of microRNAs inhibits Bcl-xL expression and potentiates sorafenib-induced apoptosis in human hepatocellular carcinoma
by Shimizu, Satoshi and Takehara, Tetsuo and Hikita, Hayato and Kodama, Takahiro and Miyagi, Takuya and Hosui, Atsushi and Tatsumi, Tomohide and Ishida, Hisashi and Noda, Takehiro and Nagano, Hiroaki and Doki, Yuichiro and Mori, Masaki and Hayashi, Norio
Journal of Hepatology, ISSN 0168-8278, 2010, Volume 52, Issue 5, pp. 698 - 704
Background & Aims Bcl-xL, an anti-apoptotic member of the Bcl-2 family, is over-expressed in human hepatocellular carcinoma, conferring a survival advantage to... 
Gastroenterology and Hepatology | Bcl-2 | Mcl-1 | Tumour | Epigenetic | Liver | TARGET | CELLS | SUPPRESSOR GENE | KINASE | IDENTIFICATION | CANCER | REPRESSES | THERAPY | GASTROENTEROLOGY & HEPATOLOGY | ASSOCIATION | MicroRNAs - therapeutic use | Niacinamide - analogs & derivatives | Oligonucleotide Array Sequence Analysis | Apoptosis - drug effects | Humans | bcl-X Protein - genetics | Antineoplastic Agents - therapeutic use | Benzenesulfonates - therapeutic use | Phenylurea Compounds | bcl-X Protein - drug effects | Benzenesulfonates - pharmacology | Carcinoma, Hepatocellular - drug therapy | Base Sequence | Carcinoma, Hepatocellular - genetics | Liver Neoplasms - pathology | Gene Expression Regulation, Neoplastic - drug effects | Pyridines - therapeutic use | Liver Neoplasms - genetics | RNA, Messenger - genetics | Enzyme Inhibitors - pharmacology | Liver Neoplasms - drug therapy | Down-Regulation - drug effects | Reverse Transcriptase Polymerase Chain Reaction | Enzyme Inhibitors - therapeutic use | Drug Synergism | Up-Regulation - drug effects | Carcinoma, Hepatocellular - pathology | RNA, Neoplasm - genetics | MicroRNAs - genetics | Pyridines - pharmacology | Cyclin G1 - genetics | Staurosporine - pharmacology
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8. Effects of natural products on Mcl-1 expression and function
by Muller, Florian and Cerella, Claudia and Radogna, Flavia and Dicato, Mario and Diederich, Marc
Current Medicinal Chemistry, ISSN 0929-8673, 11/2015, Volume 22, Issue 30, pp. 3447 - 3461
Cancer development is mostly due to a deregulation of cell death as cancer cells become resistant to apoptosis by increasing expression of anti-apoptotic... 
Mcl-1 | Natural compounds | Apoptosis | Cancer | natural compounds | DOWN-REGULATES MCL-1 | CHEMISTRY, MEDICINAL | BIOCHEMISTRY & MOLECULAR BIOLOGY | apoptosis | CELL-DEATH | TARGETING MCL-1 | INHIBITION | ACTIVATOR | BCL-2 PROTEIN FAMILY | PROSTATE-CANCER | PHARMACOLOGY & PHARMACY | cancer | TRAIL-INDUCED APOPTOSIS | HUMAN MULTIPLE-MYELOMA | SIGNAL TRANSDUCER | Proto-Oncogene Proteins c-bcl-2 - metabolism | Humans | Myeloid Cell Leukemia Sequence 1 Protein - metabolism | Biological Products - pharmacology | Molecular Structure | Cardenolides - chemistry | Gene Expression Regulation, Neoplastic - drug effects | Cardenolides - pharmacology | Myeloid Cell Leukemia Sequence 1 Protein - genetics | Drug Delivery Systems | Neoplasms - drug therapy
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9. Full Text miR‐301a promotes pancreatic cancer cell proliferation by directly inhibiting bim expression
by Chen, Zhen and Chen, Lian‐Yu and Dai, Hai‐Yan and Wang, Peng and Gao, Song and Wang, Kun
Journal of Cellular Biochemistry, ISSN 0730-2312, 10/2012, Volume 113, Issue 10, pp. 3229 - 3235
It is well known that microRNAs (miRNAs) play an important role in many diseases, including tumorigenesis. However, the mechanisms by which miRNAs regulate... 
APOPTOSIS | miR‐301a | PROLIFERATION | PANCREATIC CANCER | Bim | apoptosis | miR-301a | proliferation | Pancreatic cancer | SURVIVAL | MCL-1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOCHONDRIA | DOWN-REGULATION | ISOFORM | DEATH | MICRORNAS | CELL BIOLOGY | OVEREXPRESSION | BCL-W | Cell Proliferation | Luciferases - metabolism | Pancreatic Neoplasms - metabolism | Humans | Middle Aged | Gene Expression Regulation, Neoplastic | Male | MicroRNAs - metabolism | RNA, Neoplasm - metabolism | Bcl-2-Like Protein 11 | HEK293 Cells | Apoptosis Regulatory Proteins - genetics | Adult | Female | Membrane Proteins - metabolism | 3' Untranslated Regions | Real-Time Polymerase Chain Reaction | Proto-Oncogene Proteins - metabolism | Membrane Proteins - genetics | Pancreatic Neoplasms - pathology | Pancreatic Neoplasms - genetics | Proto-Oncogene Proteins - genetics | Blotting, Western | Apoptosis Regulatory Proteins - metabolism | RNA, Neoplasm - genetics | Aged | MicroRNAs - genetics | Apoptosis | MicroRNA | Analysis | Oncology, Experimental | Genes | Genetic research | Development and progression | Research | Cancer
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10. Full Text Programming cancer cells for high expression levels of Mcl1
by Ertel, Franziska and Nguyen, Mai and Roulston, Anne and Shore, Gordon C
EMBO reports, ISSN 1469-221X, 04/2013, Volume 14, Issue 4, pp. 328 - 336
The Bcl2 pro‐survival protein family has long been recognized for its important contributions to cancer. At elevated levels relative to pro‐apoptotic effector... 
Bcl2 | proteasome | apoptosis | mitochondria | caspase | SMALL-MOLECULE | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOCHONDRIAL MATRIX | DOWN-REGULATION | DEPENDENT APOPTOSIS | BH3 MIMETIC ABT-737 | CELL BIOLOGY | ANTI-APOPTOTIC MCL-1 | PROMOTES SURVIVAL | BCL-2 FAMILY-MEMBERS | E3 UBIQUITIN LIGASE | MEMBRANE PERMEABILIZATION | Neoplasms - metabolism | Protein Structure, Tertiary | Gene Expression | Humans | Gene Expression Regulation, Neoplastic | Molecular Targeted Therapy | Neoplasms - drug therapy | Proto-Oncogene Proteins c-bcl-2 - metabolism | Animals | Proteolysis | Myeloid Cell Leukemia Sequence 1 Protein | Proto-Oncogene Proteins c-bcl-2 - chemistry | Protein Processing, Post-Translational | Neoplasms - pathology | Proto-Oncogene Proteins c-bcl-2 - genetics | Apoptosis | Proteins | Mitochondria | Gene expression | Molecular biology | Cancer | Review
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11. Full Text Mcl-1 phosphorylation defines ABT-737 resistance that can be overcome by increased NOXA expression in leukemic B cells
by Mazumder, Suparna and Choudhary, Gaurav S and Al-harbi, Sayer and Almasan, Alexandru
Cancer Research, ISSN 0008-5472, 06/2012, Volume 72, Issue 12, pp. 3069 - 3079
ABT-737 is a small molecule Bcl-2homology (BH)-3 domain mimetic that binds to the Bcl-2 family proteins Bcl-2 and Bcl-xL and is currently under investigation... 
MULTIPLE-MYELOMA | MITOCHONDRIAL APOPTOSIS | ONCOLOGY | CASPASE-MEDIATED CLEAVAGE | PROSTATE-CANCER | DOWN-REGULATION | CHRONIC LYMPHOCYTIC-LEUKEMIA | BH3 DOMAINS | BCL-2 FAMILY | UP-REGULATION | CANCER-THERAPY | Phosphorylation | Apoptosis - drug effects | Humans | Drug Resistance, Neoplasm | Proto-Oncogene Proteins c-bcl-2 - metabolism | Bcl-2-Like Protein 11 | Biphenyl Compounds - pharmacology | Nitrophenols - pharmacology | RNA Interference | Leukemia, B-Cell - drug therapy | Antineoplastic Agents - pharmacology | Membrane Proteins - metabolism | Proto-Oncogene Proteins - metabolism | Leukemia, B-Cell - pathology | Sulfonamides - pharmacology | Piperazines - pharmacology | Proto-Oncogene Proteins c-bcl-2 - biosynthesis | Apoptosis Regulatory Proteins - metabolism | Gossypol - pharmacology | Pyrroles - pharmacology | Myeloid Cell Leukemia Sequence 1 Protein | Cell Line, Tumor | Proto-Oncogene Proteins c-bcl-2 - antagonists & inhibitors | RNA, Small Interfering | Proto-Oncogene Proteins c-bcl-2 - genetics | ABT-737 | Mcl-1 | gossypol | B-cell tumor | Noxa
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12. Full Text MiR‐139 Inhibits Mcl‐1 Expression and Potentiates TMZ‐Induced Apoptosis in Glioma
by Li, Rui‐Yan and Chen, Ling‐Chao and Zhang, Hai‐Yan and Du, Wen‐Zhong and Feng, Yan and Wang, Han‐Bing and Wen, Jin‐Qiong and Liu, Xin and Li, Xian‐Feng and Sun, Ying and Yang, Dong‐Bo and Jiang, Tao and Li, Yong‐Li and Jiang, Chuan‐Lu and CGCG
CNS Neuroscience & Therapeutics, ISSN 1755-5930, 07/2013, Volume 19, Issue 7, pp. 477 - 483
Summary Aims Mcl‐1, an antiapoptotic member of the Bcl‐2 family, is overexpressed in human glioblastoma, conferring a survival advantage to tumor cells. The... 
Mcl‐1 | Temozolomide | Glioma | miR‐139 | Apoptosis | Mcl-1 | MiR-139 | DOWN-REGULATION | miR-139 | CELL-SURVIVAL | NEUROSCIENCES | LUNG-CANCER | IN-VITRO | HEPATOCELLULAR-CARCINOMA | INVASION | GLIOBLASTOMA | PATHWAY | GROWTH | PHARMACOLOGY & PHARMACY | MALIGNANT PROGRESSION | Immunohistochemistry | Oligonucleotides - genetics | Neoplasm Transplantation | Apoptosis - drug effects | Humans | Brain Neoplasms - pathology | Antineoplastic Agents, Alkylating - pharmacology | MicroRNAs - metabolism | MicroRNAs - pharmacology | Luciferases - genetics | Paraffin Embedding | Dacarbazine - pharmacology | Glioma - pathology | Dacarbazine - analogs & derivatives | Plasmids - genetics | 3' Untranslated Regions | Real-Time Polymerase Chain Reaction | Blotting, Western | Animals | Mice, Nude | Myeloid Cell Leukemia Sequence 1 Protein - biosynthesis | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Genetic research | RNA | Gliomas | Analysis | Cellular biology
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13. Full Text PI3K/mTOR dual inhibitor NVP-BEZ235 decreases Mcl-1 expression and sensitizes ovarian carcinoma cells to Bcl-x(L)-targeting strategies, provided that Bim expression is induced
by Jebahi, A and Villedieu, M and Petigny-Lechartier, C and Brotin, E and Louis, MH and Abeilard, E and Giffard, F and Guercio, M and Briand, M and Gauduchon, P and Lheureux, S and Poulain, L
CANCER LETTERS, ISSN 0304-3835, 06/2014, Volume 348, Issue 1-2, pp. 38 - 49
We previously showed that BcI-x(L) and Mcl-1 cooperatively protect platinum-resistant ovarian cancer cells from apoptosis. Here we assessed the anticancer... 
CANCER-CELLS | INDUCED APOPTOSIS | Bim | NVP-BEZ235 | ABT-737 | BCL-2 FAMILY PROTEINS | ACQUIRED-RESISTANCE | DOWN-REGULATION | BH3 MIMETIC ABT-737 | PI3K INHIBITION | Ovarian cancer | TRANSLATIONAL CONTROL | Mcl-1 | ERK1/2 | MEK INHIBITION | ONCOLOGY | MYELOID-LEUKEMIA
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14. Full Text MicroRNA‐136 promotes lipopolysaccharide‐induced ATDC5 cell injury and inflammatory cytokine expression by targeting myeloid cell leukemia 1
by Wang, Yang and Kong, Daliang
Journal of Cellular Biochemistry, ISSN 0730-2312, 11/2018, Volume 119, Issue 11, pp. 9316 - 9326
Osteoarthritis is the most frequent chronic bone and joint diseases in older populations all over the world. Lipopolysaccharide (LPS)‐induced murine... 
microRNA‐136 | lipopolysaccharide | Wnt/β‐catenin signaling pathway | Janus kinase/signal transducer and activator of transcription signaling pathway | myeloid cell leukemia 1 | osteoarthritis | Wnt/β-catenin signaling pathway | microRNA-136 | KNEE | SURVIVAL