A systems biology understanding of the synergistic effects of arsenic sulfide and Imatinib in BCR/ABL-associated leukemia - Wikidata - wikimedia - TriplyDB

A systems biology understanding of the synergistic effects of arsenic sulfide and Imatinib in BCR/ABL-associated leukemia

A systems biology understanding of the synergistic effects of arsenic sulfide and Imatinib in BCR/ABL-associated leukemia

http://www.wikidata.org/entity/Q28387697

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Reduced reactive oxygen species-generating capacity contributes to the enhanced cell growth of arsenic-transformed epithelial cells From an old remedy to a magic bullet: molecular mechanisms underlying the therapeutic effects of arsenic in fighting leukemia Arsenic trioxide inhibits human cancer cell growth and tumor development in mice by blocking Hedgehog/GLI pathway Traditional Chinese medicine and cancer: History, present situation, and development Network-based drug discovery by integrating systems biology and computational technologies Integrated analysis of microarray data of atherosclerotic plaques: modulation of the ubiquitin-proteasome system.miRNA-21 regulates arsenic-induced anti-leukemia activity in myelogenous cell lines.Autophagy is the predominant process induced by arsenite in human lymphoblastoid cell lines Simultaneous in vivo RP-HPLC-DAD quantification of multiple-component and drug-drug interaction by pharmacokinetics, using 6,7-dimethylesculetin, geniposide and rhein as examples.Autophagy is a critical mechanism for the induction of the antileukemic effects of arsenic trioxide.miR-153 sensitized the K562 cells to As2O3-induced apoptosis.As4S4 targets RING-type E3 ligase c-CBL to induce degradation of BCR-ABL in chronic myelogenous leukemia.Arsenic sulfide as a potential anti‑cancer drug.Mutant p53 protein is targeted by arsenic for degradation and plays a role in arsenic-mediated growth suppression.Transcriptional profile of Paracoccidioides induced by oenothein B, a potential antifungal agent from the Brazilian Cerrado plant Eugenia uniflora.BCR-ABL suppresses autophagy through ATF5-mediated regulation of mTOR transcription The difference between blood-associated and water-associated herbs of Danggui-Shaoyao San in theory of TCM, based on serum pharmacochemistry.Realgar quantum dots induce apoptosis and necrosis in HepG2 cells through endoplasmic reticulum stress Alternative approaches to eradicating the malignant clone in chronic myeloid leukemia: tyrosine-kinase inhibitor combinations and beyond.Future perspectives of Chinese medical formulae: chinmedomics as an effector.Knowledge building insights on biomarkers of arsenic toxicity to keratinocytes and melanocytes Autophagic degradation of the BCR-ABL oncoprotein and generation of antileukemic responses by arsenic trioxide Arsenic suppresses cell survival via Pirh2-mediated proteasomal degradation of ΔNp63 protein.Metabolomics coupled with proteomics advancing drug discovery toward more agile development of targeted combination therapies.Exploring the ligand-protein networks in traditional chinese medicine: current databases, methods, and applications The chimeric ubiquitin ligase SH2-U-box inhibits the growth of imatinib-sensitive and resistant CML by targeting the native and T315I-mutant BCR-ABL Targeting survival pathways in chronic myeloid leukaemia stem cells Advancing drug discovery and development from active constituents of yinchenhao tang, a famous traditional chinese medicine formula.Biological responses to arsenic compounds Proteomic approaches in myeloid leukemia.Drug discovery enters a new era with multi-target intervention strategy.Targeted therapy: The new lease on life for acute promyelocytic leukemia, and beyond.Network-based drug repositioning.Potentiating therapeutic effects by enhancing synergism based on active constituents from traditional medicine.Anti-miR-21 oligonucleotide sensitizes leukemic K562 cells to arsenic trioxide by inducing apoptosis.Role of Oxidative Stress in Modulating Unfolded Protein Response Activity in Chronic Myeloid Leukemia Cell Line MicroRNA-21 is involved in X-ray irradiation resistance in K562 leukaemia cells.VEGF depletion enhances bcr-abl-specific sensitivity of arsenic trioxide in chronic myelogenous leukemia.Endoplasmic reticulum stress-mediated apoptosis in imatinib-resistant leukemic K562-r cells triggered by AMN107 combined with arsenic trioxide.Arsenite-induced autophagy is associated with proteotoxicity in human lymphoblastoid cells.

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A systems biology understanding of the synergistic effects of arsenic sulfide and Imatinib in BCR/ABL-associated leukemia

http://www.wikidata.org/entity/Q28387697

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2009 nî lūn-bûn

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2009 թվականի մարտին հրատարակված գիտական հոդված

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Jian-Hua Mao

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Jing Lu

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Lin Weng

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Qiu-Hua Huang

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Sai-Juan Chen

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Yan Zhang

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Yin-Yin Xie

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Zhu Chen

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P2860

Arsenite-induced Cdc25C Degradation is through the KEN-box and Ubiquitin-proteasome Pathway

The tumor promoter arsenite stimulates AP-1 activity by inhibiting a JNK phosphatase

Structure of the Bcr-Abl oncoprotein oligomerization domain

Structural basis for ubiquitin-mediated dimerization and activation of the ubiquitin protein ligase Cbl-b

Targeted degradation of the AML1/MDS1/EVI1 oncoprotein by arsenic trioxide

Arsenic induces apoptosis of multidrug-resistant human myeloid leukemia cells that express Bcr-Abl or overexpress MDR, MRP, Bcl-2, or Bcl-x(L)

Expression cloning for arsenite-resistance resulted in isolation of tumor-suppressor fau cDNA: possible involvement of the ubiquitin system in arsenic carcinogenesis

Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia

Systems analysis of transcriptome and proteome in retinoic acid/arsenic trioxide-induced cell differentiation/apoptosis of promyelocytic leukemia.

In vitro effect of arsenical compounds on glutathione-related enzymes.

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