Apoptosis Activator 2 - CAS 79183-19-0
Catalog number: 79183-19-0
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Apoptosis Inducer
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1.The Role of Heat Shock Protein 90B1 in Patients with Polycystic Ovary Syndrome.
Li L1,2, Mo H2, Zhang J3, Zhou Y1, Peng X1, Luo X1. PLoS One. 2016 Apr 5;11(4):e0152837. doi: 10.1371/journal.pone.0152837. eCollection 2016.
Polycystic ovary syndrome (PCOS) is a heterogenetic disorder in women that is characterized by arrested follicular growth and anovulatory infertility. The altered protein expression levels in the ovarian tissues reflect the molecular defects in folliculogenesis. To identify aberrant protein expression in PCOS, we analyzed protein expression profiles in the ovarian tissues of patients with PCOS. We identified a total of 18 protein spots that were differentially expressed in PCOS compared with healthy ovarian samples. A total of 13 proteins were upregulated and 5 proteins were downregulated. The expression levels of heat shock protein 90B1 (HSP90B1) and calcium signaling activator calmodulin 1 (CALM1) were increased by at least two-fold. The expression levels of HSP90B1 and CALM1 were positively associated with ovarian cell survival and negatively associated with caspase-3 activation and apoptosis. Knock-down of HSP90B1 with siRNA attenuated ovarian cell survival and increased apoptosis.
2.Therapeutic benefits of combined treatment with tissue plasminogen activator and 2-(4-methoxyphenyl)ethyl-Yu S1, Liu X1, Shen Y1, Xu H1, Yang Y1, Ding F2. Neuroscience. 2016 Apr 7. pii: S0306-4522(16)30061-6. doi: 10.1016/j.neuroscience.2016.04.006. [Epub ahead of print]
Tissue plasminogen activator (tPA) is the only approved therapy for acute ischemic stroke, but tPA therapy is limited by a short therapeutic window and some adverse side effects. 2-(4-Methoxyphenyl)ethyl-2-acetamido-2-deoxy-β-d-pyranoside, a salidroside analog (code-named SalA-4g), has shown potent neuroprotective effects. In this study, a rat model of embolic middle cerebral artery occlusion (MCAO) was used to mimic ischemic stroke. The embolic MCAO rats were intravenously (iv) injected with tPA alone, SalA-4g alone, or a combination of tPA and SalA-4g. Compared to treatment with tPA alone at 4h post MCAO, combined treatment with tPA at 4h post MCAO and SalA-4g starting at 4h post MCAO and continuing for 3days at an interval of 24h significantly reduced neurological deficits and infarct volume, and significantly inhibited the intracerebral bleeding, edema formation, neuronal loss, and cellular apoptosis in the ischemic brain. Our results suggested that additive neuroprotective actions of SalA-4g contributed to widening the therapeutic window of tPA therapy and ameliorating its side effects in treating MCAO rats.
3.Cleavage by Caspase 8 and Mitochondrial Membrane Association Activate Bid during TRAIL-induced Apoptosis.
Huang K1, Zhang J1, O'Neill KL1, Gurumurthy CB1, Quadros RM1, Luo X2. J Biol Chem. 2016 Apr 6. pii: jbc.M115.711051. [Epub ahead of print]
The BH3-only protein Bid is known as a critical mediator of the mitochondrial pathway of apoptosis following death receptor activation. However, since full-length Bid possesses potent apoptotic activity, the role of a caspase-mediated Bid cleavage is not established in vivo. In addition, due to the fact that multiple caspases cleave Bid at the same site in vitro, the identity of the Bid-cleaving caspase during death receptor signaling remains uncertain. Moreover, as Bid maintains its overall structure following its cleavage by caspase 8, it remains unclear how Bid is activated upon cleavage. Here, Bid-deficient (Bid KO) colon cancer cells were generated by gene editing, and were reconstituted with wild-type or mutants of Bid. While the loss of Bid blocked apoptosis following treatment by TNF-related apoptosis inducing ligand (TRAIL), this blockade was relieved by re-introduction of the wild-type Bid. In contrast, the caspase-resistant mutant BidD60E and a BH3 defective mutant BidG94E failed to restore TRAIL-induced apoptosis.
4.Factors regulating nuclear factor-kappa B activation in esophageal cancer cells: Role of bile acids and acid.
Abdel-Latif MM, Inoue H, Kelleher D, Reynolds JV1. J Cancer Res Ther. 2016 Jan-Mar;12(1):364-73. doi: 10.4103/0973-1482.174525.
AIMS: Gastroesophageal reflux disease is considered to be a major risk in the development of esophageal adenocarcinoma. Nuclear factor-kappa B (NF-κB) plays important roles in the regulation of several genes coding for cytokines, cell proliferation, and apoptosis. To understand the role of bile and acid in the causation of esophageal cancer, we have examined the effects of bile acids and acid on NF-κB activation in the esophageal epithelial cells OE33 and SKGT-4 qualitatively and quantitatively.
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