CCNDI, CDK6, p21, p53, Caspase-3 (CASP-3), Caspase-8 (CASP-8, Caspase-9 (CASP9
), BCL-2, Ataxia Telangiectasia Mutated (ATM), Ataxia Telangiectasia and Rad-3 Related (ATP), BAX, Checkpoint kinase 1-2 (CHEK1, CHEK2) and Excision repair cross-complementing I (EPCCI) gene expression analyses were performed using the StepOnePlus quantitative RTPCR system (Applied-Biosystems, USA) with respect to SYBR Green (Thermo-Scientific, USA) method.
The effects of gemcitabine and combination of FA and gemcitabine on expressions of genes are important in apoptosis including CASP3, CASP7, CASP8, CASP9
, BCL2, BAX, FAS, CYCS, TNF and PPARG, and were determined using qPCR analysis, after total RNA isolation and cDNA synthesis from control and dose group cells.
Rigorous analysis of clustering shows that 60 genes were coexpressed (AKT1, BAD, BAX, BCL2, BDNF, CASP3, CASP8, CASP9
, MYC, PIK3CD, MAPK1, MAPK10, and CYCS).
Ala28Val polymorphism (rsl052571), located in an intron of caspase-9, decreases the probability of a mild form of AP .
Activity of caspase-3 (CASP3), caspase-8 (CASP8), and caspase-9 (CASP9
) was measured using the Green Caspase Staining Kit (Promokine, Heidelberg, Germany) according to the manufacturer's protocol.
In addition, the expression of proapoptotic caspases (CASP3, CASP7, CASP8, and CASP9
) is increased, while the expression of [Bcl.sub.2] (an antiapoptotic factor) is decreased in obesity .
We first selected the 36 most important biological modules (CDK4, CDK6, CDK2AP2, BC[L.SUB.2], XIAP, BAX, CASP3, CASP8, CASP9
, FOXA2, HNF4A, EBP, HGF, NFKB2, STAT3, IL6, I[L.SUB.1]0, HIF1AN, MYC, GSK3B, TP53, PTEN, RB1, MDM2, PDGFRA, SOX2, PIK3CA, FGFR1, IGF1R, EPHA2, MET, EGFR, DDR2, KEAP1, KRAS, and AKT1) out of the whole genome for lung cancer according to .
Furthermore, EGCG and L-theanine inhibited TNF-[alpha]-induced apoptosis-related gene expression (e.g., CASP9
), and caspase activity while inhibiting TNF[alpha]-induced VCAM1, LC3A and LC3B protein expression.
Evaluation of the effects of chlorophyllin on apoptosis induction, inhibition of cellular proliferation and mRNA expression of CASP8, CASP9
, APC and [beta]-catenin.
Zhang, "Automated protein structure modeling in CASP9
by I-TASSER pipeline combined with QUARK-based ab initio folding and FG-MD-based structure refinement," Proteins, vol.
TABLA III PATRON DE LATENCIA DEL VIRUS EPSTEIN BARR Y NEOPLASIAS ASOCIADAS Latencia Genes virales Neoplasias asociadas expresados I EBNA-1 Linfoma de Burkit EBERs BARF II EBNA-1 Linfoma de Hodgkin EBERs Cancer nasofaringeo LMP-1 Linfoma periferico LMP-2 T/NK BARF III Todos EBNAs Linfomas asociados a EBERs SIDA LMP-1 Desordenes LMP-2 linfoproliferativos BARF Postransplantes TABLA IV GENES CANDIDATOS Y LINFOMAS FAMILIARES Via Genes Ciclo celular/ AICDA, BAX, BCL2,BCL2A1,BCL2L1,BCL2L2, BCL2L10, Apoptosis BCL2L11(BIM), BCL6, BCL7A, BCL7C, BCL10, CASP1, CASP14, CASP4, CASP5, CASP6, CASP7, CASP8AP2, CASP9
, CCND1, LMO2, MYC, PIM1, RIPK1, RIPK2, TP53, TP53I.
The loss of their phosphatase activity prevents the dephosphorylation of phosphatidylinositol-3,4,5-trisphosphate to phosphatidylinositol-4,5-bisphosphate, which then allows the transfer of phosphate molecule to PDK1 and AKT proteins, allowing the activation of MDM2, GSK3, P27, P21, CASP9
, BAD, FKHR, IKK, and MTOR genes (Figure 1).