Hippo signaling pathway component

The term “Hippo signaling pathway components” refers to a group of evolutionarily conserved proteins forming the core of the Hippo pathway, which is a kinase signaling cascade fundamentally regulating organ size, cell proliferation, apoptosis, tissue regeneration, and cell fate[3][6]. In mammals, the canonical core includes serine/threonine kinases MST1/2 (STK4/STK3), scaffold protein SAV1, kinases LATS1/2, adaptor protein MOB1A/B, and downstream transcriptional co-activators YAP and TAZ, which themselves interact with TEAD transcription factors to activate gene expression. Hippo pathway activity is tightly regulated by various intracellular and extracellular signals, and its dysregulation is implicated in diverse diseases, most notably cancer, but also cardiac, renal, pulmonary, hepatic, and immune diseases[3][2][1]. Several therapeutic strategies are in preclinical and clinical development, most aiming to inhibit YAP/TAZ activity or target the kinases MST1/2 and LATS1/2, with the goal of suppressing abnormal cell proliferation and tumor growth[1][2][4][6]. Direct targeting remains a challenge due to the pathway’s central role in many normal physiological functions and its complexity[2][1]. Drugs in development include kinase inhibitors, TEAD inhibitors, and agents affecting upstream regulators. Notes: - The query asks about an entire pathway, not a single molecule or receptor, so this entry is inherently broad and not a canonical “target” in the conventional therapeutic sense. - To get structured data, each component (e.g. “MST1/2 kinase”, “YAP”, “TAZ”, “TEAD transcription factor”) should ideally be catalogued separately following the conventions outlined above. - “Hippo signaling pathway component” as a singular, structured “target” should be marked as **is_incorrect: true** due to its lack of specificity; only individual components are proper molecular targets.

Other names

Hippo pathway componentHippo kinasesHippo core kinase cascadeMST1/2LATS1/2SAV1MOB1A/BYAPTAZTEAD

Inhibition of MST1/2 or LATS1/2 kinases; disruption of YAP/TAZ-TEAD interaction to prevent downstream pro-tumor transcriptional activity; phosphorylation of YAP/TAZ to inhibit nuclear localization and function