Hippo Signaling Pathway Research Reagents

MST1/2 (STK4/STK3) — The apical kinases of the Hippo core cascade, orthologous to Drosophila Hippo. MST1/2 form a complex with the scaffold protein SAV1 and undergo trans-autophosphorylation to achieve full activation. Activated MST1/2 phosphorylate LATS1/2 and MOB1 to propagate the kinase signal. MST1/2 also participate in apoptotic signaling through caspase-mediated cleavage, releasing a constitutively active kinase fragment. MST1/2 double knockout in mouse liver results in massive hepatomegaly and eventual hepatocellular carcinoma, demonstrating their tumor-suppressive function.
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LATS1/2 — AGC family serine/threonine kinases that directly phosphorylate YAP and TAZ to suppress their nuclear activity. LATS1/2 are activated by MST1/2-mediated phosphorylation of their hydrophobic motif and by MOB1 co-activator binding. LATS1/2 function as bona fide tumor suppressors; epigenetic silencing by promoter hypermethylation is observed in breast, colorectal, and astrocytoma cancers. Phospho-LATS1 (Thr1079) and phospho-LATS2 (Thr1041) antibodies serve as readouts for core cascade activation.
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MOB1 (MOB1A/MOB1B) — An essential co-activator of LATS1/2 kinases. MST1/2-mediated phosphorylation of MOB1 enhances its binding to LATS1/2, allosterically promoting LATS autophosphorylation and substrate recognition. MOB1A/B double knockout phenocopies YAP hyperactivation, confirming MOB1 as a critical tumor-suppressive node. MOB1 phosphorylation (Thr35) is a proximal readout of MST1/2 activity.
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YAP (YAP1) — The principal transcriptional co-activator downstream of the Hippo cascade. When Hippo signaling is active, LATS1/2-mediated phosphorylation of YAP at Ser127 creates a 14-3-3 binding site that sequesters YAP in the cytoplasm, and phosphorylation at Ser397 primes YAP for β-TrCP-mediated ubiquitination and degradation. When unphosphorylated, YAP enters the nucleus and partners with TEAD transcription factors to drive proliferative and anti-apoptotic gene programs. YAP amplification and nuclear overexpression are observed in hepatocellular carcinoma, ovarian cancer, and squamous cell carcinomas. Phospho-YAP (Ser127) and total YAP antibodies are standard tools for assessing pathway status by Western blot and IHC.
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TAZ (WWTR1) — A YAP paralogue and transcriptional co-activator that is regulated by LATS1/2 phosphorylation in a manner largely analogous to YAP. TAZ has both overlapping and distinct functions — it uniquely interacts with the Wnt pathway effector DVL and promotes β-catenin degradation in the cytoplasm, and it is a critical driver of mesenchymal stem cell differentiation toward osteoblast versus adipocyte lineages. TAZ gene fusions (TAZ–CAMTA1, TAZ–FOSB) are pathognomonic for epithelioid hemangioendothelioma.
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TEAD1–4 — A family of transcription factors that serve as the primary DNA-binding partners of nuclear YAP/TAZ. TEADs recognize a conserved MCAT/Muscle CAT motif and are transcriptionally inert without co-activator binding. Because TEAD–YAP interaction is essential for the oncogenic output of the pathway, the TEAD–YAP protein-protein interface has emerged as a major therapeutic target. Small-molecule TEAD palmitoylation inhibitors (e.g., IK-930, VT3989) that disrupt TEAD–YAP binding are currently in clinical trials for NF2-mutant mesothelioma and other YAP/TAZ-dependent cancers.
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NF2 (Merlin) — A FERM-domain tumor suppressor that activates the Hippo kinase cascade by recruiting LATS1/2 to the plasma membrane. NF2 biallelic inactivation is the defining genetic event in neurofibromatosis type 2 (schwannomas, meningiomas) and malignant pleural mesothelioma. NF2-null tumors exhibit constitutive nuclear YAP/TAZ activity and are prime candidates for TEAD–YAP inhibitor therapy. NF2 loss also deregulates mTORC1 and receptor tyrosine kinase signaling, underscoring its role as a multifunctional tumor suppressor.
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KIBRA (WWC1) — A WW-domain scaffolding protein that recruits and activates LATS1/2 independently of MST1/2, functioning as an alternative Hippo pathway activator. KIBRA binds Merlin (NF2) and acts cooperatively to promote LATS1/2 phosphorylation. KIBRA promoter hypermethylation is associated with B cell acute lymphoblastic leukemia and chronic lymphocytic leukemia, contributing to YAP/TAZ-driven proliferation.
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AMOT (Angiomotin) — A member of the Motin family that directly binds YAP through PPxY–WW domain interactions and sequesters it at tight junctions, independently of LATS-mediated phosphorylation. AMOT provides a cell polarity-dependent mechanism of YAP regulation and links Hippo signaling to epithelial junction integrity. AMOT also promotes LATS2 kinase activity by acting as a scaffold, making it both a direct and indirect YAP suppressor.
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2. Zanconato F, Cordenonsi M, Piccolo S. YAP/TAZ at the roots of cancer. Cancer Cell. 2016;29(6):783-803. DOI

3. Moya IM, Halder G. Hippo–YAP/TAZ signalling in organ regeneration and regenerative medicine. Nat Rev Mol Cell Biol. 2019;20(4):211-226. DOI

4. Bueno R, et al. Comprehensive genomic analysis of malignant pleural mesothelioma identifies recurrent mutations, gene fusions and splicing alterations. Nat Genet. 2016;48(4):407-416. DOI