protein
| interacting normally with PTCH |
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activating GLI1 |
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interaction with KIF3A is mediated by beta-arrestins |
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Sertoli cells coordinate DHH-dependent spermatogenesis events via PTCH1 and SMO prior to the first meiotic division and in postmeiotic (haploid) cells, particularly during the first half of spermiogenesis |
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USP8 interacting with SMO (overexpression of USP8 prevents SMO ubiquitination and elevates SMO accumulation, leading to increased HH signaling activity) |
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EVC/EVC2 complex interacts with SMO and is required for signal transduction events |
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SMO activates trimeric G proteins and CARD11-associated signaling complex, leading to NFKB1 activation, contributing to the survival of DLBCL |
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ESCRT-II complex, especially VPS36, has a special role in controlling HH signaling by targeting the membrane protein SMO for its trafficking in the absence of HH, thereby regulating HH signaling activity |
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in the absence of HH, VPS36 interacts with ubiquitylated SMO, thereby negatively regulating the accumulation of SMO on plasma membrane |
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interaction between SMO and VPS36 is mediated by the VPS36 GLUE domain, and regulated by the HH signal and SMO C-tail phosphorylation |
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bifurcation of SMO activity in HH response, with a DLG5-independent arm for suppression of GLI repressor formation and a second arm involving SMO interaction with DLG5 for GLI activation |
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activated NOTCH1 leads to pronounced accumulation of SMO within primary cilia and elevated levels of full-length GLI3 |
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DYRK1B is a critical positive regulator of HH/GLI signaling downstream of SMO |
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PTCH1/PTCH2 mediate likely secretion of a SMO-inhibitory cholesterol precursor |
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SUMO pathway promotes HH signaling by regulating SMO subcellular localization , suggesting on how sumoylation regulates membrane protein trafficking |
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. HH reciprocally controls trafficking of SMO and PTC through the SMURF family of E3 ubiquitin ligases |
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HERC4, which binds to SMO, and regulates HH signalling by controlling SMO ubiquitination and degradation |
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HERC4 acts as a tumor suppressor via destabilizing the oncoprotein SMO |
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inactivation of PTCH1 by HH likely allows a transmembrane sterol to access this seven-transmembrane site (potentially through a hydrophobic tunnel), which drives the activation of SMO |