ID:PPAL_HUMAN DESCRIPTION: RecName: Full=Lysosomal acid phosphatase; Short=LAP; EC=3.1.3.2; Flags: Precursor; CATALYTIC ACTIVITY: A phosphate monoester + H(2)O = an alcohol + phosphate. SUBCELLULAR LOCATION: Lysosome membrane; Single-pass membrane protein; Lumenal side. Lysosome lumen. Note=The soluble form arises by proteolytic processing of the membrane-bound form. PTM: The membrane-bound form is converted to the soluble form by sequential proteolytic processing. First, the C-terminal cytoplasmic tail is removed. Cleavage by a lysosomal protease releases the soluble form in the lysosome lumen. PTM: N-glycosylated. The intermediates formed during enzymatic deglycosylation suggest that all eight predicted N-glycosylation sites are used. DISEASE: Defects in ACP2 are a cause of acid phosphatase deficiency (ACPHD) [MIM:200950]. The clinical features are intermittent vomiting, hypotonia, lethargy, opisthotonos, terminal bleeding, and death in early infancy. Lysosomal acid phosphatase is deficient in cultured fibroblasts and multiple tissues. SIMILARITY: Belongs to the histidine acid phosphatase family.
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.
ModBase Predicted Comparative 3D Structure on P11117
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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.