产品名称
SFTPD human, recombinant, expressed in E. coli, ≥80% (SDS-PAGE)
biological source
human
recombinant
expressed in E. coli
assay
≥80% (SDS-PAGE)
form
liquid
mol wt
18.9 kDa (175 aa, 224-375 aa + His Tag)
packaging
pkg of 100 μg
concentration
1 mg/mL
UniProt accession no.
shipped in
dry ice
storage temp.
−70°C
Gene Information
human ... SFTPD(6441)
Biochem/physiol Actions
SFTPD (surfactant protein D) protein is thought to decrease inflammatory responses in alveolar macrophages and oxidant production, and increase apoptotic cell clearance. Elevated serum levels of this protein function as biomarker for susceptibility to COPD (chronic obstructive pulmonary disease). It is involved in the pathogenesis of COPD, and certain polymorphisms in this gene are linked with changes in its serum level and lung function. In human bronchoalveolar lavage, SFTPD is the predominant protein involved in antiviral response against seasonal strains of influenza A virus (IAV). Studies in mice show that the neck and carbohydrate recognition domain (NCRD) of this protein confers protection against allergy and respiratory syncytial virus infection. Variations in this gene are linked with lung function measures in context of tobacco smoking. Hence, this protein has potential as a biomarker for subclinical tobacco smoke-induced lung damage.
General description
SFTPD (surfactant protein D) is a Ca2+-binding, large multimeric hydrophilic protein, which is produced by type II pneumocytes and club cells. It lines the alveolar epithelium. It is a member of collectins (collagen-containing C-type lectins) which are involved in innate responses.
SFTPD, as known as Surfactant pulmonary-associated protein D, is a member of the collectin family of C-type lectins that is synthesized in many tissues including respiratory epithelial cells in the lung, and contains one C-type lectin domain and one collagen-like domain. It is humoral molecules of the innate immune system, and is considered a functional candidate in chronic periodontitis. It is also involved in the development of acute and chronic inflammation of the lung. Several human lung diseases are characterized by decreased levels of bronchoalveolar SFTPD. Recombinant human SFTPD protein, fused to His-tag at N-terminus, was expressed in E.coli.
SFTPD (surfactant protein D) encodes an extracellular soluble protein that is expressed in the mucosal membrane. The SFTPD gene is mapped to human chromosome 10q22.3.
SFTPD (surfactant protein D) encodes an extracellular soluble protein that is expressed in the mucosal membrane. The SFTPD gene is mapped to human chromosome 10q22.3.
Physical form
1 mg/mL in 20 mM Tris-HCl buffer (pH 8.0) containing 10% glycerol, and 0.4 M Urea.
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
Genetic variants of pulmonary SP-D predict disease outcome of COPD in a Chinese population.
Ou CY, et al.
Respirology, 20(2), 296-303 (2015)
Mutations flanking the carbohydrate binding site of surfactant protein D confer antiviral activity for pandemic influenza A viruses.
Nikolaidis NM, et al.
American Journal of Physiology. Lung Cellular and Molecular Physiology, 306(11), L1036-L1044 (2014)
Surfactant protein D delays Fas-and TRAIL-mediated extrinsic pathway of apoptosis in T cells.
Djiadeu P, et al.
Apoptosis, 22(5), 730-740 (2017)
Kelly A Soltysiak et al.
PloS one, 10(9), e0136699-e0136699 (2015-09-15)
Coxiella burnetii is a Gram-negative, obligate intracellular bacterium and the causative agent of Q fever. Infections are usually acquired after inhalation of contaminated particles, where C. burnetii infects its cellular target cells, alveolar macrophages. Respiratory pathogens encounter the C-type lectin
Characterization of Early Stages of Human Alveolar Infection by the Q Fever Agent Coxiella burnetii.
Amanda L Dragan et al.
Infection and immunity, 87(5) (2019-03-06)
Human Q fever is caused by the intracellular bacterial pathogen Coxiella burnetii Q fever presents with acute flu-like and pulmonary symptoms or can progress to chronic, severe endocarditis. After human inhalation, C. burnetii is engulfed by alveolar macrophages and transits
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