Four patients with BAD subsequently developed epileptic seizures (2.2% of total patients, 4.0% of patients with BAD), whereas no patients with lacunar infarction developed epileptic seizures.
Here, we show that upon HIV infection, macrophages increase the expression of BCL2, BCLXL, TREM1, mitofusin 1 (MFN1), and MFN2 and the translocation of BCL2L11 (BIM) to the mitochondria and decrease the expression of BCL2-associated agonist of cell death (BAD) and BAX while maintaining a 95% survival rate over 28 days.
Overall, this study demonstrates that increased expression of hMMP2 may attenuate the severity of diabetes by protecting islet β-cells from apoptosis through an integrin-mediated activation of the Akt/BAD pathway.
Overall, this study demonstrates that increased expression of hMMP2 may attenuate the severity of diabetes by protecting islet β-cells from apoptosis through an integrin-mediated activation of the Akt/BAD pathway.
In addition, YWHAB silencing alleviated the migration of OA‑treated VSMCs and increased translocation of the BAD protein from the cytoplasm to the mitochondria.
A wide variety of other proteins, including caspase-3, and bcl-2 family members (bcl2, bclX, MCL1, BAK, BAX, BIM, BAD) showed wide variations in expression among the different viral infections.
NPB reduced phosphorylation of BAD-Ser99 and enhanced caspase 3/7 activity with associated loss of cell viability in various human cancer cell lines derived from mammary, endometrial, ovarian, hepatocellular, colon, prostatic, and pancreatic carcinoma.
Effect of cytokine-induced killer cells combined with dendritic cells on the survival rate and expression of 14-3-3ζ and p-Bad proteins in Lewis lung cancer cell lines.
Effect of cytokine-induced killer cells combined with dendritic cells on the survival rate and expression of 14-3-3ζ and p-Bad proteins in Lewis lung cancer cell lines.
Effect of cytokine-induced killer cells combined with dendritic cells on the survival rate and expression of 14-3-3ζ and p-Bad proteins in Lewis lung cancer cell lines.
To assess the seizure-protective role of knocking out (KO) the Bad gene in a chronic epilepsy model, we used the Kcna1<sup>-/-</sup> model of epilepsy, which displays progressively increased seizure severity and recapitulates the early death seen in sudden unexplained death in epilepsy (SUDEP).
The prognostic role of a nuclear factor-kappaB (NF-κB) signature derived from GASC-BAD was tested in 530 newly diagnosed diffuse LGG patients comprised within The Cancer Genome Atlas (TCGA) database.
On comparing the best parameters of all 3 machines, the AUC of the Belin/Ambrosio enhanced ectasia total derivation (BAD-D) and the inferior-superior value (ISV) of Pentacam were statistically similar to that of the keratoconus prediction index (KPI) and keratoconus probability (Kprob) of Galilei (P = .27) and 4.5 mm root mean square per unit area (RMS/A) back of Sirius (P = .55).
RhoJ deletion in BRAF mutant melanocytes modulates the expression of the pro-apoptotic protein BAD as well as genes involved in cellular metabolism, impairing nevus formation, cellular transformation, and metastasis.
RhoJ deletion in BRAF mutant melanocytes modulates the expression of the pro-apoptotic protein BAD as well as genes involved in cellular metabolism, impairing nevus formation, cellular transformation, and metastasis.