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CASP7 — HDAC1

Text-mined interactions from Literome

Komata et al., Int J Oncol 2005 (Brain Neoplasms...) : Furthermore, caspase inhibition assay indicated that HDAC inhibitor induced apoptosis was caspase dependent ... Taken together, the HDAC inhibitors, N-butyric acid and trichostatin A, induce caspase-8- but not caspase-9 dependent apoptosis with or without p21 mediated G1 arrest in human malignant glioma cells
Sato et al., Int J Oncol 2006 (Carcinoma, Squamous Cell...) : Moreover, these events were associated with an enhancement of reactive oxygen species ( ROS ) generation and caspase-3 activation by HDAC inhibitors
Pisalyaput et al., J Neurochem 2008 : Interestingly, SAP did not induce caspase and calpain activation, suggesting that C1q neuroprotection is in distinct from caspase and calpain pathways
Norian et al., Journal of oncology 2009 : We found that HDAC inhibition in B-CLL cells led to increased TRAIL receptor expression, increased caspase activation, decreased expression of antiapoptotic regulators such as Bcl-2, and ultimately, enhanced TRAIL induced apoptosis
Cai et al., PloS one 2012 (Spinal Cord Injuries) : Taken together, it is suggested that : ( i ) in the presence of CtBP , CIBZ gene is involved in secondary injury process and trigger the activation of apoptotic caspase-3 and bax genes independent of p53 ; ( ii ) abrupt down-regulation of CtBP at 8 h is a sign of mitochondria dysfunction and the onset of cell death ; ( iii ) it could be used as an inhibitor or target drug of caspase-3 gene to improve spinal cord function
McCourt et al., Clin Cancer Res 2012 (Prostatic Neoplasms) : The histone deacetylase inhibitors ( HDACi ) , droxinostat and SAHA, also downregulated c-FLIP expression, induced caspase-8- and caspase-3/7 mediated apoptosis, and increased apoptosis in bicalutamide treated cells
Gu et al., Anticancer Drugs 2012 (Neuroblastoma) : Our studies showed that inhibition of HDAC decreased NB proliferation, and induced caspase activity and G1 growth arrest