ID:CLN5_HUMAN DESCRIPTION: RecName: Full=Ceroid-lipofuscinosis neuronal protein 5; Short=Protein CLN5; Flags: Precursor; INTERACTION: P05787:KRT8; NbExp=1; IntAct=EBI-1043514, EBI-297852; SUBCELLULAR LOCATION: Lysosome. TISSUE SPECIFICITY: Ubiquitous. PTM: Glycosylated. DISEASE: Defects in CLN5 are the cause of neuronal ceroid lipofuscinosis type 5 (CLN5) [MIM:256731]; also known as Finnish variant late-infantile neuronal ceroid lipofuscinosis (vLINCL). A form of neuronal ceroid lipofuscinosis. Neuronal ceroid lipofuscinoses are progressive neurodegenerative, lysosomal storage diseases characterized by intracellular accumulation of autofluorescent liposomal material, and clinically by seizures, dementia, visual loss, and/or cerebral atrophy. The lipopigment patterns observed most often in neuronal ceroid lipofuscinosis type 5 comprise mixed combinations of granular, curvilinear, and fingerprint profiles. SIMILARITY: Belongs to the CLN5 family. SEQUENCE CAUTION: Sequence=AAC27614.1; Type=Erroneous initiation; Note=Translation N-terminally shortened; WEB RESOURCE: Name=NCL CLN5; Note=Neural Ceroid Lipofuscinoses mutation db; URL="http://www.ucl.ac.uk/ncl/cln5.shtml"; WEB RESOURCE: Name=GeneReviews; URL="http://www.ncbi.nlm.nih.gov/sites/GeneTests/lab/gene/CLN5";
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
Pfam Domains: PF15014 - Ceroid-lipofuscinosis neuronal protein 5
ModBase Predicted Comparative 3D Structure on O75503
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.