Genome-wide CRISPR/Cas9 screens enable the identification of actionable vulnerabilities of oral squamous cell carcinoma, and their unique dependencies on YAP1 and WWTR1 of the Hippo pathway.
Host restriction factors that block cross-species transmission also play a role in limiting the replication of highly-adapted HIV-1 in IFN-stimulated cells.
The protein p53 negatively impacts the ability of a CRISPR screen to discriminate between essential and non-essential genes, hence, p53 status should be considered in these screens.
The HOXA9 reporter and genetic screens facilitated the functional interrogation of the HOXA9 regulome and advanced our understanding of the molecular regulation network in HOXA9-driven leukemia.
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.
CRISPR/Cas9 genome-wide screens using sterol-sensitive endogenous HMG-CoA reductase (HMGCR) reporter identify the sterol-responsive RNF145 and gp78 as independently responsible for sterol-accelerated degradation of HMGCR, the rate-limiting enzyme of cholesterol biosynthesis.
TRAF3, a negative regulator of noncanonical NF-κB signaling, maintains epithelial cell quiescence at confluence, and its loss triggers upregulation of immunity genes and prevents entry into G0 at high cell density.
Functional genomic screening reveals new synthetic lethality with and modes of resistance to epidermal growth factor receptor (EGFR) targeted therapy in EGFR-mutant human lung cancer.
The initiation of human genome replication requires the six-subunit origin recognition complex (ORC) and CDC6, with ORC playing additional roles during mitosis and in organization of the cell nucleus.
