Tag: Cancer biology

Post-translational modifications are essential regulators of cell-cycle progression. Learn how phosphorylation, ubiquitination, acetylation, SUMOylation, methylation, and other PTMs control CDKs, cyclins, checkpoints, DNA replication, mitosis, and protein degradation.

Post-translational modifications are essential regulators of apoptosis. Learn how phosphorylation, ubiquitination, acetylation, SUMOylation, methylation, and other PTMs control p53, BCL-2 proteins, caspases, mitochondrial apoptosis, and cell survival.

Protein succinylation is a metabolic post-translational modification that connects succinyl-CoA metabolism with protein function, mitochondrial activity, epigenetic regulation, gene expression and cellular homeostasis.

Protein S-glutathionylation is a reversible cysteine modification that connects glutathione metabolism with redox signaling, oxidative stress responses, protein function, mitochondrial biology and disease.

Lysine malonylation is a metabolic post-translational modification that connects malonyl-CoA metabolism with protein function, mitochondrial activity, epigenetic regulation and cellular homeostasis.

Protein lactylation is an emerging post-translational modification that connects lactate metabolism with protein regulation, gene expression, inflammation, cellular signaling and disease.

Protein citrullination is a calcium-dependent post-translational modification that converts arginine into citrulline. Explore PAD enzymes, histone citrullination, NETosis, inflammation, rheumatoid arthritis, autoimmunity, cancer, and citrullination proteomics.

Protein ADP-ribosylation is an important post-translational modification that uses NAD+ to regulate proteins and cellular pathways. Explore mono- and poly-ADP-ribosylation, PARP enzymes, DNA repair, chromatin regulation, cancer, metabolism, inflammation, and cell death.

Replication stress occurs when DNA replication forks stall or collapse, generating genomic instability and driving tumour evolution. Through ATR–CHK1 signalling, fork protection and homologous recombination repair, cells stabilise damaged forks and prevent catastrophic chromosomal breakage.

XIAP is the most potent endogenous inhibitor of caspases and a central regulator of apoptosis and immune signalling. Through its BIR domains and RING ubiquitin ligase activity, XIAP blocks caspase‑3, caspase‑7 and caspase‑9 while modulating NF‑κB pathways, making it a key player in cancer, inflammation and immune disorders.

Survivin (BIRC5) is a tumour‑specific IAP that integrates apoptosis suppression with essential mitotic functions. As part of the chromosomal passenger complex, Survivin ensures proper chromosome segregation while stabilising anti‑apoptotic pathways, making it a central driver of tumour progression and therapy resistance.

Livin (ML‑IAP) is a tumour‑specific inhibitor of apoptosis that blocks caspase activity and ubiquitinates pro‑apoptotic proteins. Its splice variants, Livin‑α and Livin‑β, differ in potency, and its unique ability to switch from anti‑apoptotic to pro‑apoptotic after cleavage makes Livin a key regulator of tumour survival and therapy resistance.

Timely protein degradation is essential for orderly cell-cycle progression. Explore key cell-cycle regulators, their degradation mechanisms, and how their turnover controls G1/S transition, mitosis, chromosome segregation and mitotic exit.

Autophagosomes are double‑membrane vesicles that capture cytoplasmic material for lysosomal degradation. Formed from expanding phagophores and marked by LC3 lipidation, autophagosomes are central to autophagy, enabling cells to recycle nutrients, remove damaged organelles and maintain homeostasis. Their dysfunction contributes to neurodegenerative, metabolic and cancerous diseases.

Cdc25 phosphatases activate CDKs to drive both the G1–S and G2–M transitions. By removing inhibitory phosphates from CDK1 and CDK2, Cdc25 triggers DNA replication and mitotic entry. Checkpoint kinases such as Chk1 inhibit Cdc25 during DNA damage, while Cdc25 overexpression promotes genomic instability and contributes to tumour progression.