SFTPB Protein, Human, Recombinant (His)

Catalog No. TMPY-06810

Pulmonary surfactant-associated protein B, also known as SFTPB and SP-B, contains one saposin A-type domain and three saposin B-type domains. SP-B is produced primarily by alveolar type II cells (AEC2) but also by nonciliated respiratory epithelial cells lining distal portions of the respiratory tract. Its secretion promotes alveolar homeostasis, stabilizing lipid layers and lowering surface tension at the air-liquid interface in the peripheral air spaces. Alveolar SP-B influences surfactant formation, effector cell functions, and innate host defense. Deficiency is associated with respiratory distress syndrome (RDS), pulmonary surfactant metabolism dysfunction 1 (SMDP1), and other human lung diseases. Gene addition and editing therapies show promise by complementing SP-B expression in AEC2s, restoring the phenotypic defect in vitro and in vivo.

SFTPB Protein, Human, Recombinant (His)

Catalog No. TMPY-06810

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100 μg	$801	7-10 days

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Product Information

Biological Activity	Activity testing is in progress. It is theoretically active, but we cannot guarantee it. If you require protein activity, we recommend choosing the eukaryotic expression version first.
Description	Pulmonary surfactant-associated protein B, also known as SFTPB and SP-B, contains one saposin A-type domain and three saposin B-type domains. SP-B is produced primarily by alveolar type II cells (AEC2) but also by nonciliated respiratory epithelial cells lining distal portions of the respiratory tract. Its secretion promotes alveolar homeostasis, stabilizing lipid layers and lowering surface tension at the air-liquid interface in the peripheral air spaces. Alveolar SP-B influences surfactant formation, effector cell functions, and innate host defense. Deficiency is associated with respiratory distress syndrome (RDS), pulmonary surfactant metabolism dysfunction 1 (SMDP1), and other human lung diseases. Gene addition and editing therapies show promise by complementing SP-B expression in AEC2s, restoring the phenotypic defect in vitro and in vivo.
Species	Human
Expression System	CHO Cells
Tag	C-His
Accession Number	P07988
Synonyms	SP-B,SMDP1,SFTP3,SFTB3,PSP-B
Construction	A DNA sequence encoding the Human SFTPB (NP_000533.4) (Trp25-Ser381) was expressed with a polyhistidine tag at the C-terminus. Predicted N terminal: Trp 25
Protein Purity	≥ 95% as determined by SDS-PAGE
Molecular Weight	41.04 kDa (predicted); 45 kDa (reducing conditions)
Endotoxin	< 1.0 EU/μg of the protein as determined by the LAL method.
Formulation	Lyophilized from a solution filtered through a 0.22 μm filter, containing PBS, pH 7.4. Typically, a mixture containing 5% to 8% trehalose, mannitol, and 0.01% Tween 80 is incorporated as a protective agent before lyophilization.
Reconstitution	A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.
Stability & Storage	It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.
Shipping	In general, Lyophilized powders are shipping with blue ice.
Research Background	Pulmonary surfactant-associated protein B, also known as SFTPB and SP-B, contains one saposin A-type domain and three saposin B-type domains. SP-B is produced primarily by alveolar type II cells (AEC2) but also by nonciliated respiratory epithelial cells lining distal portions of the respiratory tract. Its secretion promotes alveolar homeostasis, stabilizing lipid layers and lowering surface tension at the air-liquid interface in the peripheral air spaces. Alveolar SP-B influences surfactant formation, effector cell functions, and innate host defense. Deficiency is associated with respiratory distress syndrome (RDS), pulmonary surfactant metabolism dysfunction 1 (SMDP1), and other human lung diseases. Gene addition and editing therapies show promise by complementing SP-B expression in AEC2s, restoring the phenotypic defect in vitro and in vivo.