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GenomicsInhibition of ADSS2-mediated de novo AMP biosynthesis resensitizes acute myeloid leukemia to BH3 mimetics
Inhibition of ADSS2-mediated de novo AMP biosynthesis resensitizes acute myeloid leukemia to BH3 mimetics
PRJNA1175730 | ENA
GenomicsInhibition of ADSS2-mediated de novo AMP biosynthesis resensitizes acute myeloid leukemia to BH3 mimetics [scRNA-seq]
Inhibition of ADSS2-mediated de novo AMP biosynthesis resensitizes acute myeloid leukemia to BH3 mimetics [scRNA-seq]
PRJNA1176037 | ENA
ProteomicsClonal plasma cells in AL amyloidosis are dependent on pro-survival BCL-2 family proteins and sensitive to BH3 mimetics alone and in combination with front-line therapies
Amyloid light chain amyloidosis (AL) is an incurable protein misfolding disorder characterized by the production of amyloidogenic immunoglobulin light chains by clonal populations of plasma cells. These abnormal light chains accumulate as amyloid fibrils in vital organs and cause multi-organ dysfunc...
ORGANISM(S): Homo sapiens (Human) 
2022-10-03 | PXD024119 | Pride
Al amyloidosis bcl-2 apoptosis bh3 bortezomib proteasome inhibition 
UnknownHuman herpesvirus 8 interferon regulatory factor-mediated BH3-only protein inhibition via Bid BH3-B mimicry.
Not available
S-EPMC3369933 | biostudies-literature
GenomicsMitophagy promotes resistance to BH3 mimetics in acute myeloid leukemia
Mitophagy promotes resistance to BH3 mimetics in acute myeloid leukemia
PRJNA756171 | ENA
TranscriptomicsTranscription profiling of human cell cancer line treated with bortezomib or Eeyarestatin I (EerI) reveals ERAD inhibitors integrate ER stress with an epigenetic mechanism to activate BH3 only protein NOXA in cancer cells
The ubiquitin-proteasome system (UPS) has recently emerged as a major target for drug development in cancer therapy. The proteasome inhibitor bortezomib has clinical activity in multiple myeloma and mantle cell lymphoma. Here we report that Eeyarestatin I (EerI), a chemical inhibitor that blocks ER-...
ORGANISM(S): Homo sapiens 
2009-02-28 | E-GEOD-14003 | biostudies-arrayexpress
UnknownAMPK inhibition sensitizes acute leukemia cells to BH3 mimetic-induced cell death.
Not available
S-EPMC11043078 | biostudies-literature
TranscriptomicsInhibition of ADSS2-mediated de novo AMP biosynthesis resensitizes acute myeloid leukemia to BH3 mimetics
De novo purine synthesis is required to promote tumor growth; however, its role in therapy resistance remains elusive. Here, through a dynamic BH3-priming based CRISPR-Cas9 screen, we found that deletion of ADSS2, which encodes for an enzyme functioning in de novo AMP synthesis, re-sensitizes drug r...
ORGANISM(S): Homo sapiens 
2025-11-21 | GSE280009 | GEO
TranscriptomicsMCL1 inhibitor induces apoptosis in Anaplastic Large Cell Lymphoma and in Primary Effusion Lymphoma
Overexpression of antiapoptotic BCL2 family proteins occurs in various hematologic malignanices and contributes to leukemogenesis by inhibiting the apoptotic machinery of the cells. BH3 mimetics provide an option for medication, with venetoclax as the first drug applied for chronic lymphocytic leuke...
ORGANISM(S): Homo sapiens 
2021-12-31 | E-MTAB-10903 | biostudies-arrayexpress
ProteomicsStructural Insights into Chemoresistance Mutants of BCL-2 and their Targeting by Stapled BAD BH3 Helices
BCL-2 is a central regulator of apoptosis that inhibits cell death by sequestering pro-apoptotic BH3 alpha-helices within a hydrophobic surface groove. While venetoclax, a BH3-mimetic drug, has transformed the treatment of BCL-2–driven malignancies, its efficacy is increasingly limited by acquired r...
ORGANISM(S): Homo sapiens (Human) 
2025-09-30 | PXD062817 | Pride
Bcl-2 Venetoclax Bh3 inhibition Resistance mutation Hydrogen/deuterium exchange mass spectrometry Apoptotic regulation Bad Hdx-ms Stapled peptide 
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