• Considering our previous results with cfDNA in EGFR TKI resi

  2024-10-10

  

  Considering our previous results with cfDNA in EGFR TKI-resistant NSCLC patients and growing evidence about different mutations in the ALK kinase domain as responsible for acquired resistance to ALK TKIs, we planned this study. Even if a next-generation sequencing approach after PD during crizotini

• Recently a Phase III study demonstrated that alectinib

  2024-10-10

  

  Recently, a Phase III study demonstrated that alectinib, the second-generation ALK inhibitor, might have a better response to ALK-rearrangement patients than crizotinib [10]. Should alectinib replace crizotinib as the frontline treatment for ALK-rearranged patients? Or should those patients be trea

• In this study we demonstrated

  2024-10-10

  

  In this study, we demonstrated that DRR1 protein level in GBM tissues was significantly higher compared to normal Estradiol tissues. This data suggested that DRR1 might play a role in the tumorigenesis of glioma. To investigate whether DRR1 could accurately predict the outcome in patients with glio

• The present study determined the effect of

  2024-10-10

  

  The present study determined the effect of DCA on VSMC calcification in vitro and in atherosclerotic ApoE-/- mice in vivo. We found that pcr kit non-toxic concentrations of DCA, did not affect VSMC viability, induced calcification of VSMC in culture and increased atherosclerotic vascular calcificat

• br AHR mediates TCDD toxicity

  2024-10-10

  

  AHR mediates TCDD toxicity and wasting syndrome TCDD causes numerous toxicities in laboratory animals, including teratogenesis, hepatic steatosis, thymic atrophy, immune dysfunction and a lethal wasting syndrome [17]. The dose-dependent sensitivity to TCDD-induced toxicities varies widely among l

• In terms of the ring

  2024-10-09

  

  In terms of the ring B C5′ position, while C5′-F (compound ) was tolerated, C5′-Me (compound ) and C5′-Cl (compound ) substitutions resulted in a loss in potency. However, the C5′-OMe substitution (compound ) resulted in a ∼3-fold increase in potency compared to . Modeling suggested a pseudo hydroge

• br STAR Methods br Author

  2024-10-09

  

  STAR★Methods Author Contributions Acknowledgments We thank Antony M. Dean for initial discussions and encouragement concerning ancestral sequence reconstruction. We also thank Natalie K. Goto for constructive criticism concerning the manuscript, Steven M. Sine for providing pkm2 receptor s

• neurokinin receptor antagonist Princen Panier specifically a

  2024-10-09

  

  Princen, 2012, Panier, 2013 specifically address the issue of ACE using the commercial database AMADEUS. However, both studies focus only on corporate leverage and the ACE in Belgium. Due to the lack of a counterfactual, these authors consider firms in other European countries, e.g., France, as a co

• Direct inhibition of LO activity by BRP is

  2024-10-09

  

  Direct inhibition of 5-LO activity by BRP-187 is clearly evident in cell-free assays using PMNL homogenates and isolated human recombinant 5-LO as enzyme source. In such assays, pure FLAP inhibitors like MK886 are inactive [9], [10], [29], [44]. Wash-out experiments and studies using the nonionic de

• Thus one possible target for CRPC treatment is

  2024-10-09

  

  Thus one possible target for CRPC treatment is the enzyme 17,20-lyase, which plays a crucial role in androgen biosynthesis. This is because inhibition of 17,20-lyase would be expected to decrease serum androgen levels secreted not only by the testes but also by the adrenal glands.7, 8, 9 In recent

• Double immunofluorescence staining of Gas and Axl with neuro

  2024-10-09

  

  Double immunofluorescence staining of Gas6 and Axl with neuronal specific nuclear protein (NeuN), glial fibrillary acidic protein (GFAP), and ionized calcium-binding adaptor molecule 1 (Iba-1), demonstrated that Gas6 and Axl are expressed by neurons, astrocytes and microglia/macrophages (Fig. 2). In

• To identify the kinase s mediating

  2024-10-09

  

  To identify the kinase(s) mediating H3.3S31 phosphorylation, we devised a 96-well-plate-compatible immunostaining assay, with prostaglandin synthase specific for H3.3S31ph, and utilized it to screen both a Qiagen siRNA library covering 720 human kinases and a kinase inhibitor library (Selleck) cont

• Because of the formation of phosphoenzyme intermediates

  2024-10-09

  

  Because of the formation of phosphoenzyme intermediates, the enzymatic Dihydroeponemycin of P-ATPases can be divided into steps that include a kinase activity, by which an aspartate residue on the enzyme is phosphorylated, and a phosphatase activity, by which the phosphoenzyme is dephosphorylated.

• Suspecting that ACL might regulate the expression

  2024-10-09

  

  Suspecting that ACL might regulate the expression or activity of myogenic transcription factors, Das knocked down MyoD and found that such intervention abolished the effect of ACL on fast MyHC expression and that, conversely, MyoD overexpression partially rescued reduced fast MyHC expression caused

• br Author contributions br Conflicts

  2024-10-09

  

  Author contributions Conflicts of interest The authors declare no competing financial interests. Acknowledgement This work was supported by grants from the Deutsche Forschungsgemeinschaft (Sonderforschungsbereich/Transregio 166–Project C1 and grant CA 1014/1-1 to D.C.) and the IZKF Würzbur

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