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The interacting proteins of PTPN23 on A375 cells were identified by affinity proteomics
ORGANISM(S): Homo sapiens (Human) 
2025-01-08 | PXD051577 | Pride
Protein expression levels between control shRNA group and PTPN23 shRNA group
ORGANISM(S): Homo sapiens (Human) 
2025-01-08 | PXD051603 | Pride
In our study, a CRISPR screen of acute myeloid leukemia cells identifies protein tyrosine phosphatase non-receptor type 23 (PTPN23) as essential for survival. Loss of PTPN23 activates nuclear factor-kappa B, apoptotic, necroptotic, and pyroptotic pathways by causing the accumulation of death recepto...
ORGANISM(S): Homo Sapiens 
2024-10-15 | PXD056836 |
Phosphorylated protein levels between control shRNA group and PTPN23 shRNA group
ORGANISM(S): Homo sapiens (Human) 
2025-01-08 | PXD051604 | Pride
Cell death plasticity is crucial for modulating tissue homeostasis and immune responses, but our understanding of the molecular components that regulate cell death pathways to determine cell fate remains limited. Here, a CRISPR screen of acute myeloid leukemia cells identifies protein tyrosine phosp...
ORGANISM(S): Homo sapiens 
2024-10-16 | GSE272123 | GEO
Exosomes play pleiotropic tumor-promoting functions and are originated from a diversion of endocytic pathway. In late endocytic trafficking, multivesicular bodies (MVBs) are directed to lysosomes for degradation or secreted as exosomes. However, the mechanism controlling different fates of MVBs rema...
ORGANISM(S): Homo sapiens (Human) 
2025-01-24 | PXD050029 | Pride
PTPN23-dependent ESCRT machinery functions as a cell death checkpoint in restraining multiple cell death pathways
Signalling by target-derived neurotrophins is essential for the correct development of the nervous system and its maintenance throughout life. Several aspects concerning the lifecycle of neurotrophins and their receptors, tropomyosin receptor kinases (Trks) and p75NTR, have been characterised over t...
ORGANISM(S): Mus musculus (Mouse) 
2020-05-26 | PXD016190 | Pride
Aberrant overexpression or activation of EGFR drives the development of non-small cell lung cancer (NSCLC) and acquired resistance to EGFR tyrosine kinase inhibitors (TKIs) by secondary EGFR mutations or c-MET amplification/activation remains as a major hurdle for NSCLC treatment. We previously iden...
ORGANISM(S): Homo sapiens (Human) 
2023-10-09 | PXD025361 | Pride
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