Bort/venetoclax promote synergistic cell death through inducing expression of apoptotic and DNA damage response markers as well as inhibitor of NF-κB but suppressed regulators for cell cycle progression in sLCLs.

<p>sLCL 381 and sLCL 421 were treated with combination of bortezomib (0, 1, 2, 4, 8, 16, 32, and 64 nM) and venetoclax (0, 1.25, 2.5, 5, 10, 20 μM) for 24 hours and stained by MTT solution. OD570 nm and OD630 nm were measured, and cell viability was plotted. <b>(a)</b> Percentages...

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Bibliographic Details
Main Author:	Kam Pui Tam (19746865) (author)
Other Authors:	Jia Xie (247149) (author), Rex Kwok Him Au-Yeung (19746868) (author), Alan K. S. Chiang (8677455) (author)
Published:	2024
Subjects:	Biochemistry Medicine Microbiology Cell Biology Molecular Biology Pharmacology Immunology Cancer Mental Health Hematology Infectious Diseases Virology transplant lymphoproliferative disorder latent membrane protein distinct latency patterns cause synergistic killing b signaling pathway associated hemophagocytic lymphohistiocytosis nf -&# 954 b &# 945 bortezomib potently induced xlink "> epstein latent viral proteins ebv nuclear antigen cell cycle arrest bortezomib prevented lmp 2 causing g1 venetoclax inhibited bcl viral proteins &# 954 inhibited mcl venetoclax targets venetoclax decreased taken together scid mice proteasome system proteasome inhibitor phosphorylated p65 host cells either lmp dependent manner data corroborated cyclin d1 apoptotic initiator 2 upregulated 2 simultaneously 2 inhibitor 2 family 001 ).
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Bort/venetoclax promote synergistic cell death through inducing expression of apoptotic and DNA damage response markers as well as inhibitor of NF-κB but suppressed regulators for cell cycle progression in sLCLs.

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