protein
| phosphorylation target of Aurora-A kinase (AURKA)(and this phosphorylation plays a role of the centrosomal localization of LATS2) |
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AR-interacting protein |
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LATS1 and LATS2 are novel HSP90AA1 clients and HSP90AA1 inhibitors can disrupt the LATS tumor suppressor pathway in cancer cells |
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AMOT activate LATS2 through a novel conserved domain that binds and activates LATS2 |
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binding between WWC1 and LATS2 requires the N-terminal 86 AAs of WWC1 and the PPPY motif and AAs 667–788 in LATS2 |
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interacting with FOXP3 (LATS2 induction required binding of FOXP3 to a specific sequence in the LATS2 promoter, and this interaction contributed to FOXP3-mediated growth inhibition of tumor cells) |
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LATS2 kinase is a novel regulator of SNAI1 protein level, subcellular localization, and thus, activity |
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LATS2 modulates ESR1-regulated gene transcription, through direct and/or indirect interactions with ESR1 |
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involved in phosphorylation of AMOT130, which is a key feature that enables it to inhibit YAP1-dependent signaling and cell growth |
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AMOT is a direct substrate of LATS1/LATS2 mediating functions of the Hippo pathway in endothelial cell migration and angiogenesis |
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LATS1, LATS2 can synergize with F-actin perturbations by phosphorylating free AMOT130 to keep it from associating with F-actin |
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LATS1 and LATS2 phosphorylate CDC26 to modulate assembly of the tetratricopeptide repeat subcomplex of APC/C |