Electron tomography and biochemical approaches demonstrate a direct role for WDR35, beyond integrity of the IFT-A holocomplex, in the formation and fusion of electron-dense-coated vesicles to the ciliary sheath and pocket for delivery of cargos necessary for axoneme elongation.

PASK phosphorylates Wdr5 to trigger epigenetic changes at lineage specifying promoters resulting in transcriptional derepression and differentiation of stem or progenitor cells.

RNA binding is a key input of an active chromatin complex and maintenance of stem cell fate.

The chromatin regulator WDR5 is a regulator of translation, and small molecule inhibitors or degraders of WDR5 can be used to treat triple-negative breast cancer.

The protein stability of WDR5, the core component of TrxG complex, is controlled by the ubiquitin ligase RNF220, which involves in the maintenance of Hox patterns in mouse hindbrain.

Analysis of the action of WDR5 inhibitors in leukemia cells reveals decreased ribosome inventory, impaired protein synthesis, induction of nucleolar stress, and activation of p53 via alternative splicing of MDM4.

Differences in promoter affinity and MYC levels explain distinct expression profiles induced by physiological and oncogenic MYC.

Soluble Fas ligand interacts specifically with tumor necrosis factor receptor superfamily (TNFRSF)10B, also known as death receptor 5, exacerbating arthritis in a Fas-independent manner.

Interaction of oncoprotein transcription factor MYC with chromatin-associated protein host cell factor–1 controls expression of genes important for ribosome biogenesis and mitochondrial vigor, loss of which promotes tumor regression.

Stem cell heterogeneity is progressively built in proliferating population by the action of mitochondrial glutamine metabolism that opposes the cell cycle-linked self-renewal network to generate differentiation-competent progenitors.