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CASP3Critical Assessment in Structure Prediction (third experiment)
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According to the qPCR results, when the cells were treated with the I[C.sub.50] dose of gemcitabine, the expression of CASP3 (5.01 fold) and FAS (52.8 fold) genes were significantly upregulated.
Genes AKT1, BAD, BAX, BCL2, CASP3, CASP8, CASP9, MYC, PIK3CD, MAPK1, MAPK10, and CYCS are commonly expressed in the cluster of colorectal cancer, neuronal signaling pathway, neuronal death, amytrophic lateral aclerosis, and tuberculosis [51].
Buns et al., "Common variants in CASP3 confer susceptibility to Kawasaki disease," Human Molecular Genetics, vol.
This apoptosis is driven by the activation of CASP3 in the inhibitory GABAergic interneurons of the superficial dorsal horn and causes the loss of these neurons, the decrease of the spinal inhibition, and the appearance of neuropathic pain.
Caspases play an essential role in apoptosis, since they are initiators (CASP9, CASP8) as well as effectors (CASP3).
In the analysis of apoptosis-related genes, which also influences the number of cells and early embryo development, the 5% [O.sub.2] group had a lower abundance of transcripts of apoptosis regulatory genes such as CASP3, HSPD1, BAX, MORF4L2, and PLAC8.
Moreover, we demonstrated that Dioscin displayed anticancer activity via up-regulating expression of TP53, BAX and CASP3 protein, as well as down-regulating BCL2 in Bel-7402 cells.
The mRNA expression of caspase-3 ( Casp3 ), Bcl2-associated X protein ( Bax ), and B-cell lymphoma-2 ( Bcl2 ) were detected with PCR.
To identify the BHD mutation, systematic sequence analysis of the coding exons and intron splice sites of CASP3, LRP2BP and UFSP2 located in the linked region was conducted.
EPOR, MAPK14, BCL2L1, KRT18, PTPN6, CASP3, TGFBR2, AR, and CASP7 were genes in the five motifs with the highest SMD scores, and some of them are already known to be gastric cancer related.
Consistent with 15 nM LBH589 being a sublethal concentration based on the absence of morphological cell apoptotic features, no detectable loss of cell number, and similar proportion of early apoptotic cells to DMSO control following 48 hours culture, our gene expression data demonstrated increased expression of antiapoptotic genes (BIRC3, BCL2L2, and CFLAR) and decreased expression of proapoptotic genes (CASP3, BCL2L11, CARD8, CASP6, BNIP1, BCLAF1, CASP2, and APAF1) following LBH589 treatment (Figure 3).
The up-regulated genes include HIAP1, CRAF1, TRAF6, CASP1, CASP2, CASP3, CASP4, HPRT, GADD45, MCL-1, NIP1, BCL2L2, TRAP3, GSTP1, DAXX, PIG11, UBC, PIG3, PCNA, CDC10, JNK1 and RBP2.