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.

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.

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.

Loss of membrane-bound ICAM-1, overexpression of soluble ICAM-1 or ILKAP activity in tumor cells induce resistance to antigen-specific cytotoxic T-cell-mediated killing independently from regulating antigen presentation, PD-L1 expression, IFN-γ, or TNF-α responsiveness.

An easy-to-implement antibody validation pipeline addresses the reproducibility crisis resulting from the use of non-specific antibodies.

CRISPR/Cas9 screens reveal a role for the ubiquitin ligase substrate adaptor DCAF15 in the immune surveillance of cancer cells by natural killer cells.

A mechanistic link between TLE3 loss and glucocorticoid receptor-mediated androgen receptor inhibitor resistance supports the rationale to target GR during anti-hormonal treatment in castrate-resistant prostate cancer.

Secreted effector proteins of Toxoplasma gondii parasites create a supportive immune environment in mice, allowing individually less fit mutants to thrive and evade detection by in vivo CRISPR screens.

A genome-wide CRISPR/Cas9 knockout screening approach identified C/EBPδ as transcriptional regulator of the alarmins S100A8 and S100A9 during differentiation of monocytes and inflammatory processes in vivo.

Heparan sulfates in the vessel wall bind and regulate signaling from the megakaryocyte/platelet-specific inhibitory receptor G6b-B, a critical regulator of platelet homeostasis.