MARCH5 mediates a pathway driving MCL1 degradation in response to cellular stress, which sensitizes to BH3 mimetic drugs targeting BCLXL and provides a broadly effective therapeutic strategy for solid tumors.
Targeting the CRL5 ubiquitin ligase complex in combination with CDK9 or MCL1 inhibition could combat innate and acquired resistance of cancer cells to MCL1-targeting therapeutics.
Obligate intracellular Chlamydia secrete a deubiquitinating enzyme (Cdu1) into the membrane of the Chlamydia-containing vacuole to deubiquitinate selected host proteins and support the survival of the bacteria during genital infection.
The uniparental inheritance of mammalian mitochondria results from elimination of paternal mitochondria by a mitophagic process that requires the E3 ubiquitin ligases PARKIN and MUL1.
The interface formed where Smc3p and Mcd1p bind each other regulates cohesin DNA binding and cohesion by a mechanism independently from its putative role as a DNA exit gate.
Controlled neo-glycosylation of antigens can influence intracellular routing of antigens and the nature and strength of immune response, and should therefore be considered as a major determinant in the design of vaccines against cancer and infectious diseases.
An unbiased forward genetic screen identified genes in Mycobacterium tuberculosis that are required for fatty acid import when the bacterium is residing within macrophages.
A multi-transcriptional CDKs inhibitor suppresses MYC and induces regression of ovarian tumors, indicating that targeting CDK7, 12, 13 with THZ1 may be an effective approach for treating MYC-dependent malignancies.
During ES cell differentiation, Yap1 directly regulates apoptosis-related genes like Bcl-2 and Mcl-1 to attenuate apoptosis and promote cell survival to allow for successful cell fate changes.
