Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.10.2 (focal adhesion kinase)
 44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

P210BCR-ABL counteracted against the complementary effect of XPB on DNA repair when ultraviolet (UV)-sensitive 27-1 cells were treated with UV or cisplatin but not with hydrogen peroxide. Wortmannin, an inhibitor of PI3 kinase did not affect its anti-repair effect. Enhanced recruitment of p44 with TFIIH after cisplatin treatment is inhibited by the expression of P210BCR-ABL in a kinase activity-dependent manner. Although purified TFIIH from P210BCR-ABL expressor and non-expressor showed almost no difference in molar ratio of each component, the in vitro activity of TFIIH was decreased by 5-10% in repair assay but was increased by more than two-fold in transcription assay.
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PMID:TFIIH functions are altered by the P210BCR-ABL oncoprotein produced on the Philadelphia chromosome. 1160 Jan 36

Recently, it was shown that both Bcr and Bcr-Abl can interact with xeroderma pigmentosum group B (XPB/ERCC3), a protein implicated in DNA repair after UV-induced damage. To further analyze the effect of Bcr-Abl on the DNA damage response, we used cell lines stably transfected with the BCR-ABL gene and their parental counterparts (MBA-1 versus MO7E and Bcr-AblT1 versus 4A2(+)-pZAP) and several assays reflecting DNA repair: the comet assay, a radioimmunoassay for cyclobutane pyrimidine dimers, and clonogenic assays. After exposure to UVC (0.5-5.0 joules m(-2)), the Comet assay demonstrated greater efficiency of DNA repair in the BCR-ABL-positive cells (both MBA-1 and Bcr-AblT1) when compared with their parental counterparts. Furthermore, there was less production of the UV-induced DNA adduct-cyclobutane pyrimidine dimers-as well as a more rapid rate of disappearance of these adducts and greater UV survival (clonogenic assays) in MBA-1 cells as compared with MO7E cells. Apoptosis (annexin V-FITC/propidium iodide staining) was markedly reduced in the BCR-ABL-positive cells. These results indicate that BCR-ABL confers enhanced resistance to UV radiation-induced damage and increased efficiency of DNA repair and that these changes are associated with a protective antiapoptotic effect.
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PMID:Impact of p210(Bcr-Abl) on ultraviolet C wavelength-induced DNA damage and repair. 1450 64

The BCR-ABL oncogene encodes an in-frame fusion protein containing N-terminal sequences derived from Bcr and C-terminal sequences derived from Abl. Bcr contains a centrally located Rho-specific guanine nucleotide exchange factor (RhoGEF) domain that is retained within p210 Bcr-Abl. Although this domain is subject to autoinhibition in the context of Bcr, here we show that it is constitutively activated in p210 Bcr-Abl. p210 Bcr-Abl can stimulate RhoA activation independently of its tyrosine kinase activity, and mutations within the RhoGEF domain that are predicted to eliminate RhoGEF activity inhibit RhoA activation. The RhoGEF mutant of p210 Bcr-Abl does not affect the tyrosine kinase activity of the molecule, nor the ability of p210 Bcr-Abl to interact with XPB through the RhoGEF domain. Despite retaining normal levels of tyrosine kinase activity, the RhoGEF mutant of p210 Bcr-Abl is impaired in transforming activity as measured by anchorage-independent growth. However, the mutant is still able to confer the phenotype of growth factor independence in myeloid cells, suggesting that some, but not all parameters of p210 Bcr-Abl transformation, are dependent upon a catalytically active RhoGEF domain. Collectively, these observations identify a gain-of-function activity attributable to the RhoGEF domain of p210 Bcr-Abl that is required to support the transformed phenotype.
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PMID:The RhoGEF domain of p210 Bcr-Abl activates RhoA and is required for transformation. 1792 31

The objective of this study was to investigate microtensile bond strength (MTBS) and interfacial adaptation (IA) of bulk-fill restorative systems bonded to dentin in Class-I-preparations. Box-shaped preparations (4-mm-long, 3-mm-wide, 2-mm-high) made in extracted molars, and Teflon matrix with the same dimensions positioned over the occlusal surface were restored, providing a total of 4-mm composite depth using three bulk-fill restorative systems: Tetric EvoCeram Bulk Fill with Tetric N-Bond (TEC/TNB), SureFil SDR Flow with XP Bond (SDR/XPB) and Filtek Bulk Fill Flowable Restorative with Scotchbond Universal (FBF/SBU); or incrementally restored with a conventional restorative system: Herculite Classic with OptiBond FL (HER/OBF). The specimens were sectioned into beams and the MTBS measured after 24-hours or one-year storage. For evaluation of IA, round-tapered tooth preparations (3-mm-diameter, 1.5-mm-deep) were made, restored with each material and their cross-sectional images were obtained after 24-hours using optical coherence tomography (OCT). The gap percentage for each restoration system was calculated using image analysis software. MTBS for both storage periods: HER/OBF=TEC/TNB=SDR/XPB>FBF/SBU (ANOVA, Tukey's post-hoc, P<0.05) differed significantly among groups, which values were significantly reduced after one-year. SDR/XPB showed comparatively lesser gap formation at the tooth-interface after 24 hours (ANOVA, Dunnett's T3 post-hoc, P<0.05). For deeper restorations, bond strength of TEC/TNB and SDR/XPB can be equal to that of HER/OBF after 24-hours and one-year; however, in a shallower preparation, SDR/XPB showed greater initial interfacial adaptation.
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PMID:Evaluation of bulk-fill systems: microtensile bond strength and non-destructive imaging of marginal adaptation. 3008 53