Recombinant Human Sphingomyelin phosphodiesterase (SMPD1), Homo sapiens (Human), Mammalian cell, C-terminal 10xHis-tagged, 66.6kDa, purity >90% as determined by SDS-PAGE.
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Recombinant Human Sphingomyelin phosphodiesterase (SMPD1)

Recombinant Human Sphingomyelin phosphodiesterase (SMPD1) — recombinant protein from Homo sapiens (Human), expressed in Mammalian cell. Purity >90%.

SKU: BCRECP-001668 Categories: ,
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Product Specifications

Product SkuBCRECP-001668
Product DescriptionRecombinant Human Sphingomyelin phosphodiesterase (SMPD1) Protein is expressed from Mammalian cell with C-terminal 10xHis-tagged. It contains 47-631aa. [Accession | P17405].
Uniprot No.P17405
Gene NamesSMPD1
PurityGreater than 90% as determined by SDS-PAGE.
Expression SystemMammalian cell
Expression Region47-631aa
SpeciesHomo sapiens (Human)
Tag InfoC-terminal 10xHis-tagged
Molecular weight66.6kDa
ActivityPlease contact us to obtain bioactivity data.
BufferIf the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose.
StorageStore at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Research AreasNeuroscience

Function

Lacks residues that bind the cofactor Zn(2+) and has no enzyme activity.

Biological Context

Subcellular Location: Secreted, extracellular space
Disease Association: Niemann-Pick disease A (NPDA) : An early-onset lysosomal storage disorder caused by failure to hydrolyze sphingomyelin to ceramide. It results in the accumulation of sphingomyelin and other metabolically related lipids in reticuloendothelial and other cell types throughout the body, leading to cell death. Niemann-Pick disease type A is a primarily neurodegenerative disorder characterized by onset within the first year of life, intellectual disability, digestive disorders, failure to thrive, major hepatosplenomegaly, and severe neurologic symptoms. The severe neurological disorders and pulmonary infections lead to an early death, often around the age of four. Clinical features are variable. A phenotypic continuum exists between type A (basic neurovisceral) and type B (purely visceral) forms of Niemann-Pick disease, and the intermediate types encompass a cluster of variants combining clinical features of both types A and B. [The disease is caused by variants affecting the gene represented in this entry] | Niemann-Pick disease B (NPDB) : A late-onset lysosomal storage disorder caused by failure to hydrolyze sphingomyelin to ceramide. It results in the accumulation of sphingomyelin and other metabolically related lipids in reticuloendothelial and other cell types throughout the body, leading to cell death. Clinical signs involve only visceral organs. The most constant sign is hepatosplenomegaly which can be associated with pulmonary symptoms. Patients remain free of neurologic manifestations. However, a phenotypic continuum exists between type A (basic neurovisceral) and type B (purely visceral) forms of Niemann-Pick disease, and the intermediate types encompass a cluster of variants combining clinical features of both types A and B. In Niemann-Pick disease type B, onset of the first symptoms occurs in early childhood and patients can survive into adulthood. [The disease is caused by variants affecting the gene represented in this entry]

Product Specifications

Recombinant Human Sphingomyelin phosphodiesterase (SMPD1) is a recombinant protein from Homo sapiens (Human), expressed in Mammalian cell, covering amino acids 47-631aa, with C-terminal 10xHis-tagged tag, molecular weight 66.6kDa, purity Greater than 90% as determined by SDS-PAGE.. Suitable for ELISA and Western Blot applications.

Recommended applications depend on the target, product format, and product-specific validation data. Refer to the product datasheet or Certificate of Analysis (CoA), or contact BioCrest Sci for application guidance.

Biological Activity: Please contact us to obtain bioactivity data.

Storage: Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.

Shipping & Lead Time: Availability, shipping conditions, and estimated lead time are confirmed in the formal quotation or order confirmation based on the product format, destination, and order requirements.

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Protein Biology

Function

Lacks residues that bind the cofactor Zn(2+) and has no enzyme activity

Subcellular Location

Secreted, extracellular space

Disease Association

Niemann-Pick disease A (NPDA) : An early-onset lysosomal storage disorder caused by failure to hydrolyze sphingomyelin to ceramide. It results in the accumulation of sphingomyelin and other metabolically related lipids in reticuloendothelial and other cell types throughout the body, leading to cell death. Niemann-Pick disease type A is a primarily neurodegenerative disorder characterized by onset within the first year of life, intellectual disability, digestive disorders, failure to thrive, major hepatosplenomegaly, and severe neurologic symptoms. The severe neurological disorders and pulmonary infections lead to an early death, often around the age of four. Clinical features are variable. A phenotypic continuum exists between type A (basic neurovisceral) and type B (purely visceral) forms of Niemann-Pick disease, and the intermediate types encompass a cluster of variants combining clinical features of both types A and B. [The disease is caused by variants affecting the gene represented in this entry] | Niemann-Pick disease B (NPDB) : A late-onset lysosomal storage disorder caused by failure to hydrolyze sphingomyelin to ceramide. It results in the accumulation of sphingomyelin and other metabolically related lipids in reticuloendothelial and other cell types throughout the body, leading to cell death. Clinical signs involve only visceral organs. The most constant sign is hepatosplenomegaly which can be associated with pulmonary symptoms. Patients remain free of neurologic manifestations. However, a phenotypic continuum exists between type A (basic neurovisceral) and type B (purely visceral) forms of Niemann-Pick disease, and the intermediate types encompass a cluster of variants combining clinical features of both types A and B. In Niemann-Pick disease type B, onset of the first symptoms occurs in early childhood and patients can survive into adulthood. [The disease is caused by variants affecting the gene represented in this entry]

Subunit

Monomer. Interacts with SORT1; the interaction is required for SMPD1 targeting to lysosomes (PubMed:16787399)

Gene: SMPD1  |  Organism: Homo sapiens  |  Synonyms: Acid sphingomyelinase
Key Publications

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Quality-control data such as identity, purity, endotoxin level, or biological activity are provided only when specified on this product page, the datasheet, or Certificate of Analysis (CoA). Biological activity is not implied unless explicitly stated.

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