36 results on '"Turcq, Béatrice"'
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2. Data from Evidence that Resistance to Nilotinib May Be Due to BCR-ABL, Pgp, or Src Kinase Overexpression
3. Supplementary Table 1 from Evidence that Resistance to Nilotinib May Be Due to BCR-ABL, Pgp, or Src Kinase Overexpression
4. Supplementary Figure 1 from Evidence that Resistance to Nilotinib May Be Due to BCR-ABL, Pgp, or Src Kinase Overexpression
5. Supplementary Table 1 from Evidence that Resistance to Nilotinib May Be Due to BCR-ABL, Pgp, or Src Kinase Overexpression
6. Supplementary Figure 1 from Evidence that Resistance to Nilotinib May Be Due to BCR-ABL, Pgp, or Src Kinase Overexpression
7. ANTIMETABOLIC COOPERATIVITY WITH THE CLINICALLY-APPROVED L-ASPARAGINASE AND TYROSINE KINASE INHIBITORS TO ERADICATE CML STEM CELLS
8. 3e colloque de recherche fondamentale en oncologie pédiatrique
9. Antimetabolic cooperativity with the clinically approved kidrolase and tyrosine kinase inhibitors to eradicate cml stem cells
10. Inhibition of DDR1 enhances in vivo chemosensitivity in KRAS-mutant lung adenocarcinoma
11. A genome‐scale CRISPR knock‐out screen in chronic myeloid leukemia identifies novel drug resistance mechanisms along with intrinsic apoptosis and MAPK signaling
12. The Expression of Myeloproliferative Neoplasm-Associated Calreticulin Variants Depends on the Functionality of ER-Associated Degradation
13. Novel analytical methods to interpret large sequencing data from small sample sizes
14. CRISPR-Cas9 genome editing induces megabase-scale chromosomal truncations
15. Dasatinib-Loaded Erythrocytes Trigger Apoptosis in Untreated Chronic Myelogenous Leukemic Cells: A Cellular Reservoir Participating in Dasatinib Efficiency
16. A new mechanism of resistance to ABL1 tyrosine kinase inhibitors in a BCR-ABL1-positive cell line
17. Loss of mutL homolog-1 (MLH1) expression promotes acquisition of oncogenic and inhibitor-resistant point mutations in tyrosine kinases
18. A Single Nucleotide Polymorphism in cBIM Is Associated with a Slower Achievement of Major Molecular Response in Chronic Myeloid Leukaemia Treated with Imatinib
19. α-Defensin 1-3 And α-Defensin 4 as Predictive Markers of Imatinib Resistance and Relapse in CML Patients
20. Evidence that Resistance to Nilotinib May Be Due to BCR-ABL, Pgp, or Src Kinase Overexpression
21. Multidrug resistance gene (MDR1) polymorphisms are associated with major molecular responses to standard-dose imatinib in chronic myeloid leukemia
22. Proteomic analysis of an imatinib-resistant K562 cell line highlights opposing roles of heat shock cognate 70 and heat shock 70 proteins in resistance
23. Heat Shock Protein 70 over Expression Is Associated to Imatinib Resistance in Chronic Myelogenous Leukemia.
24. The Proteome Analysis of an Imatinib-Resistant Cell Line Identifies Changes in Molecular Chaperones Such as Heat Shock Proteins (Hsp): A Possible New Mechanism of Imatinib Resistance.
25. Characterization of the genomic organization of the region bordering the centromere of chromosome V of Podospora anserina by direct sequencing
26. Glycolipid Intermembrane Transfer Is Accelerated by HET-C2, a Filamentous Fungus Gene Product Involved in the Cell−Cell Incompatibility Response†
27. HET-E and HET-D Belong to a New Subfamily of WD40 Proteins Involved in Vegetative Incompatibility Specificity in the Fungus Podospora anserina
28. Vegetative incompatibility in filamentous fungi: a roundabout way of understanding the phenomenon
29. MOD-D, a Gα Subunit of the Fungus Podospora anserina, Is Involved in Both Regulation of Development and Vegetative Incompatibility
30. Use of a Linear Plasmid Containing Telomeres as an Efficient Vector for Direct Cloning in The Filamentous FungusPodospora anserina
31. A Mutation in an HSP90 Gene Affects the Sexual Cycle and Suppresses Vegetative Incompatibility in the Fungus Podospora anserina
32. An additional copy of the adenylate cyclase-encoding gene relieves developmental defects produced by a mutation in a vegetative incompatibility-controlling gene in Podospora anserina
33. A gene responsible for vegetative incompatibility in the fungus Podospora anserina encodes a protein with a GTP-binding motif and Gβ homologous domain
34. Vegetative incompatibility in filamentous fungi: het genes begin to talk
35. repa, a repetitive and dispersed DNA sequence of the filamentous fungusPodospora anserina
36. The ura5 gene of the filamentous fungus Podospora anserina: nucleotide sequence and expression in transformed strains
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