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SFTPB encodes the pulmonary-associated surfactant protein B (SPB), an amphipathic surfactant protein essential for lung function and homeostasis after birth. Additionally we are shipping SFTPB Kits (60) and SFTPB Proteins (14) and many more products for this protein.
Showing 10 out of 106 products:
Human Polyclonal SFTPB Primary Antibody for IHC (p), IHC - ABIN269321
Guo, Kazadaeva, Ortega, Manjunath, Desai: Trinucleotide repeat containing 6c (TNRC6c) is essential for microvascular maturation during distal airspace sacculation in the developing lung. in Developmental biology 2017
Human Polyclonal SFTPB Primary Antibody for IHC, WB - ABIN4891754
Mayor, Finch, Zehr, Morselli, Neinast, Frank, Hahner, Wang, Rakheja, Palmer, Rosenfeld, Savani, Clegg: Maternal high-fat diet is associated with impaired fetal lung development. in American journal of physiology. Lung cellular and molecular physiology 2015
TGF beta (show TGFB1 Antibodies) markedly decreased expression of SP-A, SP-B, SP-C (show SFTPC Antibodies), fatty acid synthase (show FASN Antibodies), and the phospholipid transporter ABCA3 (show ABCA3 Antibodies). However, TGF beta (show TGFB1 Antibodies) increased protein levels of SP-D (show SFTPD Antibodies) with little change in mRNA levels.
Surfactant protein B suppresses lung cancer progression by inhibiting secretory phospholipase A2 (show YWHAZ Antibodies) activity and arachidonic acid production.
SP-A (+186A/G) and SP-B (1580C/T) polymorphisms are strongly associated with the risk of respiratory distress syndrome (RDS (show PRPH2 Antibodies)) in preterm infants. Notably, reduced serum SP-A levels were correlated with a high risk of RDS (show PRPH2 Antibodies) and may serve as novel biomarkers for RDS (show PRPH2 Antibodies) detection and monitoring.
Differences were found regarding SPA and pro-SPB expression in the vast majority of subjects: in some lungs, SPA was more expressed whereas in others pro-SPB showed an higher degree of immunoreactivity. The expression of both surfactant proteins was not strictly correlated with gestational age.
There is no significant association between the gene polymorphism of the R236C site in exon 7 of SP-B gene and the incidence ofneonatal respiratory distress syndrome (NRDS) in Han populations in that region.
Rare mutations in surfactant-associated genes contribute to neonatal respiratory distress syndrome. The frequency of mutations in these genes in the Chinese population is unknown. We resequenced all exons of the surfactant protein-B (SFTPB) and we did not find any rare mutations in SFTPB
mice with SP-B-C allele are more susceptible to S. aureus pneumonia than mice with SP-B-T allele, and that CMC2.24 attenuates lung injury thus reducing mortality.
In term newborns with pneumonia, SP-B increases with respect to total phospholipids, and disaturated-phosphatidylcholine (show SGMS2 Antibodies) and is turned over at a faster rate.
SP-B -18C/A and 1580C/T polymorphisms are associated with bronchopulmonary dysplasia
These results demonstrate for the first time that human SP-B C allele is more susceptible to bacterial pneumonia than SP-B T allele in vivo.
In triple KO mice, the HO-induced lung injury was associated with decreased surfactant protein (SP) A (show SFTPA1 Antibodies) and SPC (show SFTPC Antibodies) but not SPB and SPD (show SFTPD Antibodies) expression.
Surfactant protein B had decreased levels in influenza A virus PR8-infected cells, which was confirmed by immunoblotting and immunofluorescence assays.
macrophages participate in the repression of SFTPB expression by LPS (show TLR4 Antibodies), and that macrophage-released cytokines (including TNF (show TNF Antibodies)) regulate the transcription factor CEBPB (show CEBPB Antibodies)
ErbB4 regulates the expression of surfactant protein B in fetal lung maturation, helping to prepare for the fetal-neonatal transition.
The stimulatory effects of estrogen on Sftpb are under transcriptional control of ErbB4 (show ERBB4 Antibodies).
SP-B contributes to innate host defense of the lung by supplementing the nonoxidant antimicrobial defenses of alveolar macrophages
DNA methylation and chromatin modifications cooperate with Nkx2-1 to regulate Sftpb gene cell specific expression.
formation of the intersubunit disulfide bridge is not critical for SP-B function
The late asthmatic response is linked with increased surface tension and reduced surfactant protein B in mice.
Data show that detergent-solubilized surfactant protein B (SP-B) indicate the presence of 10 nm ring-shaped particles.
Data suggest that transient exposure of surfactant to polymers like hyaluronan (HA) could be a promising strategy for the production of more efficient therapeutic surfactants SP-A (show SFTPA1 Antibodies), SP-B and SP-C (show SFTPC Antibodies) preparations.
Data indicate that in the background of phosphatidylcholine (POPC) membranes pulmonary surfactant protein SP-B exhibits a certain level of selectivity for anionic fluorescent phospholipids over the corresponding zwitterionic analogues.
SP-B and SP-C (show SFTPC Antibodies) proteins promote the formation of proteolipid channels in which lipid molecules are functionally involved.
Palmitoylation is key for the functional cooperation of SP-C with SP-B that enables cholesterol-containing surfactant films to reach very low tensions under compression.
Surfactant protein SP-B promoted film formation and reextension to lower surface tensions than SP-C (show SFTPC Antibodies).
The role of the SP-B NH(2) terminus in the formation and stability of cylindrical structures, specifically the distribution of lipid stack height, width, and density with four SP-B truncation peptides, was studied.
SP-B is unlikely to affect uptake of surfactant
The presence of phosphatidylglycerol iz required for SP-B to acquire the appropriate tertiary folding.
SFTPB is located on pig chromosome 3, and is secreted by pulmonary alveolar type II epithelial cells. It is down-regulated during Actinobacillus pleuropneumoniae lung infection.
Measurements of the depth of SP-B(CTERM) indicated the peptide center positions ~8A more deeply than the phosphate headgroups, a topology that may allow the peptide to promote functional lipid structures without causing micellization upon compression.
results suggest the hydrophobic surfactant protein, SP-B, protects alveolar surfactant phospholiopids from hydrolysis mediated by multiple sPLA(2 (show PLA2G2A Antibodies)) in both vesicles (alveolar subphase) and monomolecular films (air-liquid interface)
The hydrophobic surfactant proteins SP-B and SP-C (show SFTPC Antibodies) induce formation of bicontinuous inverse cubic phases.
Reactive oxygen species inactivation of lipid extract surfactant B (SP-B) biophysical activity appears to involve modification of a maximum of three amino acids: Trp9, Met29, and Met65.
This gene encodes the pulmonary-associated surfactant protein B (SPB), an amphipathic surfactant protein essential for lung function and homeostasis after birth. Pulmonary surfactant is a surface-active lipoprotein complex composed of 90% lipids and 10% proteins which include plasma proteins and apolipoproteins SPA, SPB, SPC and SPD. The surfactant is secreted by the alveolar cells of the lung and maintains the stability of pulmonary tissue by reducing the surface tension of fluids that coat the lung. The SPB enhances the rate of spreading and increases the stability of surfactant monolayers in vitro. Multiple mutations in this gene have been identified, which cause pulmonary surfactant metabolism dysfunction type 1, also called pulmonary alveolar proteinosis due to surfactant protein B deficiency, and are associated with fatal respiratory distress in the neonatal period. Alternatively spliced transcript variants encoding the same protein have been identified.
18 kDa pulmonary-surfactant protein
, 6 kDa protein
, pulmonary surfactant-associated protein B
, pulmonary surfactant-associated proteolipid SPL(Phe)
, surfactant associated protein B
, surfactant pulmonary-associated protein B
, surfactant, pulmonary-associated protein B
, surfactant protein B
, surfactant, pulmonary-associated protein B L homeolog