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http://purl.uniprot.org/citations/34395437http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/34395437http://www.w3.org/2000/01/rdf-schema#comment"The speckle-type POZ protein (SPOP) functions as a guardian of genome integrity and controls transcriptional regulation by functioning as a substrate adaptor for CUL3/RING-type E3 ubiquitin ligase complexes. SPOP-containing CUL3 complexes target a myriad of DNA-binding proteins involved in DNA repair and gene expression, and as such, are essential modulators of cellular homeostasis. GLI transcription factors are effectors of the Hedgehog (HH) pathway, a key driver of tissue morphogenesis and post-developmental homeostasis that is commonly corrupted in cancer. CUL3-SPOP activity regulates amplitude and duration of HH transcriptional responses by controlling stability of GLI family members. SPOP and GLI co-enrich in phase separated nuclear droplets that are thought to serve as hot spots for CUL3-mediated GLI ubiquitination and degradation. A similar framework exists in Drosophila, in which the Hedgehog-induced MATH (meprin and traf homology) and BTB (bric à brac, tramtrack, broad complex) domain containing protein (HIB) targets the GLI ortholog Cubitus interruptus (Ci) for Cul3-directed proteolysis. Despite this functional conservation, the molecular mechanisms by which HIB and SPOP contribute to Drosophila and vertebrate HH signaling differ. In this mini-review we highlight similarities between the two systems and discuss evolutionary divergence in GLI/Ci targeting that informs our understanding of how the GLI transcriptional code is controlled by SPOP and CUL3 in health and disease."xsd:string
http://purl.uniprot.org/citations/34395437http://purl.org/dc/terms/identifier"doi:10.3389/fcell.2021.710295"xsd:string
http://purl.uniprot.org/citations/34395437http://purl.uniprot.org/core/author"Ogden S.K."xsd:string
http://purl.uniprot.org/citations/34395437http://purl.uniprot.org/core/author"Umberger P.A."xsd:string
http://purl.uniprot.org/citations/34395437http://purl.uniprot.org/core/date"2021"xsd:gYear
http://purl.uniprot.org/citations/34395437http://purl.uniprot.org/core/name"Front Cell Dev Biol"xsd:string
http://purl.uniprot.org/citations/34395437http://purl.uniprot.org/core/pages"710295"xsd:string
http://purl.uniprot.org/citations/34395437http://purl.uniprot.org/core/title"SPOP and CUL3 Modulate the Sonic Hedgehog Signal Response Through Controlled Degradation of GLI Family Transcription Factors."xsd:string
http://purl.uniprot.org/citations/34395437http://purl.uniprot.org/core/volume"9"xsd:string
http://purl.uniprot.org/citations/34395437http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/34395437
http://purl.uniprot.org/citations/34395437http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/34395437
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http://purl.uniprot.org/uniprot/#_Q9VFP2-mappedCitation-34395437http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34395437
http://purl.uniprot.org/uniprot/#_Q9V475-mappedCitation-34395437http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34395437
http://purl.uniprot.org/uniprot/Q02936http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/34395437
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http://purl.uniprot.org/uniprot/P19538http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/34395437