Sodium phenylbutyrate, an HDAC (histone deacetylase) inhibitor, has been shown to cause cellular differentiation, growth arrest, and apoptosis in certain cells. Sodium phenylbutyrate has been reported to cause cell growth arrest at the G1 phase and induce apoptosis through activation of JNK. Studies suggest that Sodium Phenylbutyrate also acts as a chemical chaperone by causing a reduction of the load of mutant and mislocated proteins retained in the endoplasmic reticulum (ER). Other experiments have noted that Sodium Phenylbutyrate demonstrates neuroprotective capabilities by attenuating infarction volume, apoptosis, hemispheric swelling and improving neurological status in a murine model of hypoxia-ischemia. Moreover, this agent has been shown to suppress ER-mediated apoptosis by initiating factor 2α phosphorylation, caspase-12 activation, and CCAAT/enhancer-binding protein homologous protein induction.
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See how others have used Sodium phenylbutyrate. Click on the entry to view the PubMed entry .
PMID: # 26999661
Cao, AL. et al. 2016. Ursodeoxycholic acid and 4-phenylbutyrate prevent endoplasmic reticulum stress-induced podocyte apoptosis in diabetic nephropathy. Laboratory investigation; a journal of technical methods and pathology.
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Bobak, Y. et al. 2016. Arginine deprivation induces endoplasmic reticulum stress in human solid cancer cells. Int. J. Biochem. Cell Biol.. 70: 29-38.
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Zhou, Y. et al. 2016. Porcine Circovirus 2 Deploys PERK Pathway and GRP78 for Its Enhanced Replication in PK-15 Cells. Viruses. 8:
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Tao, K. et al. 2016. Salidroside Protects Against 6-Hydroxydopamine-Induced Cytotoxicity by Attenuating ER Stress. Neuroscience bulletin. 32: 61-9.
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Rekha, RS. et al. 2015. Phenylbutyrate induces LL-37-dependent autophagy and intracellular killing of Mycobacterium tuberculosis in human macrophages. Autophagy. 11: 1688-99.
PMID: # 24140860
Jiang, W. et al. 2013. Differential regulation of human cathelicidin LL-37 by free fatty acids and their analogs. Peptides. 50: 129-38.
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Yu, W. et al. 2011. Heat shock protein 90 inhibition results in altered downstream signaling of mutant KIT and exerts synergistic effects on Kasumi-1 cells when combining with histone deacetylase inhibitor. Leukemia research. 35: 1212-8.
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