Note: In the NCBI Build 36 reference assembly, there were four SFTPA genes on chromosome 10, with the SFTPA1/SFTPA2 gene pair being centromeric to a SFTPA1B/SFTPA2B pair. In June 2009, the Genome Reference Consortium determined that the duplicated region containing one of these gene pairs is in error, and thus, only one SFTPA1/SFTPA2 pair is present in the GRCh37 reference assembly. The HUGO Gene Nomenclature Committee (HGNC) retired the symbol SFTPA1B, because its sequence is redundant with SFTPA1. [13 Feb 2013 ...
TY - JOUR. T1 - Glucocorticoid inhibition of human SP-A1 promoter activity in NCI-H441 cells. AU - Hoover, Russell R.. AU - Thomas, Klaus H.. AU - Floros, Joanna. PY - 1999/5/15. Y1 - 1999/5/15. N2 - Glucocorticoids have complex effects on human surfactant protein (SP) SP-A1 and SP-A2 gene expression that occur at both transcriptional and post-transcriptional levels. In the lung adenocarcinoma cell line NCI-H441, dexamethasone causes a dose-dependent decrease in total SP-A mRNA levels and inhibits SP-A gene transcription. In this study, a deletional analysis of the SP-A1 promoter was performed in order to identify cis-acting elements that mediate dexamethasone responsiveness in NCI-H441 cells. The region -32/+63 relative to the start of SP-A1 transcription mediated both basal promoter activity and dexamethasone repression of transcription. Removal of the region +18/+63 abolished dexamethasone responsiveness, indicating that sequences within this region are necessary for the inhibitory effect. ...
PURPOSE: We evaluated allele frequencies and distribution of surfactant protein A2(SP-A2) in Korean neonates in order to estimate the prevalence of RDS, to find out new SP-A alleles, and to establish new steroid therapy. METHODS: Genomic DNA was extracted from 71 neonates and served as a template in PCR for genotype analysis. SP-A gene-specific amplications and gene-specific allele determinations were performed using PCR-cRFLP methods. RESULTS: The distribution for the alleles of the SP-A2 gene in the study population was 1A, 1A0, 1A1, 1A2, 1A3, 1A5, 1A6, 1A7, 1A8, 1A9, 1A11, 1A12. The specific frequencies for the alleles of the SP- A2 gene in the study population were : 1A=11.3%, 1A0=38%, 1A1=12.7%, 1A2=9.2%, 1A5=15.5%, 1A7= 2.9%, 1A8=4.9%, 1A9=2.2%, others=3.3%. CONCLUSION: The frequency of 1A0 was higher than the other SP-A2 alleles in Korean neonates. This finding suggests that the prevalence of RDS in Korea may be low compared with other countries. However, this finding also suggests that ...
Dr. Ledfords current work in the area of pulmonary surfactant immunobiology combines her knowledge of mouse genetics, pulmonary disease models and immune function regulation and focuses on understanding the role of Surfactant Protein-A (SP-A) and how it regulates signaling pathways within various immune cell populations. Specifically, she is interested in how SP-A regulates degranulation, either directly or indirectly, of two important cell types in asthma: mast cells and eosinophils. More recently, Dr. Ledfords research has focused on understanding how genetic variation within human SP-A2 alters functionality of the protein in relation to eosinophil activities and how this translates to characteristics observed in human asthma.. ...
The surfactant protein (SP-A) receptor SP-R210 has been shown to increase phagocytosis of SP-A-bound pathogens and to modulate cytokine secretion by immune cells. SP-R210S isoforms, splicing of small exons generates alternate forms of the unique carboxy-terminal domain name of Myo18A in macrophages [6]. Moreover, recent work offered in abstract form suggested that alternate splicing introduces […]. ...
The precise mechanisms that lead to parturition are incompletely defined. Surfactant protein-A (SP-A), which is secreted by fetal lungs into amniotic fluid (AF) near term, likely provides a signal for parturition; however, SP-A-deficient mice have only a relatively modest delay (~12 hours) in parturition, suggesting additional factors. Here, we evaluated the contribution of steroid receptor coactivators 1 and 2 (SRC-1 and SRC-2), which upregulate SP-A transcription, to the parturition process. As mice lacking both SRC-1 and SRC-2 die at birth due to respiratory distress, we crossed double-heterozygous males and females. Parturition was severely delayed (~38 hours) in heterozygous dams harboring SRC-1/-2-deficient embryos. These mothers exhibited decreased myometrial NF-κB activation, PGF2α, and expression of contraction-associated genes; impaired luteolysis; and elevated circulating progesterone. These manifestations also occurred in WT females bearing SRC-1/-2 double-deficient embryos, ...
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Surfactant protein A is an innate immune system collectin. It is water-soluble and has collagen-like domains similar to SP-D. It is part of the innate immune system and is used to opsonize bacterial cells in the alveoli marking them for phagocytosis by alveolar macrophages. SP-A may also play a role in negative feedback limiting the secretion of pulmonary surfactant. SP-A is not required for pulmonary surfactant to function but does confer immune effects to the organism. The role of Surfactant protein A (or SP-A) in childbirth is indicated in studies with mice. Mice which gestate for 19 days typically show signs of SP-A in amniotic fluid at around 16 days. If SP-A is injected into the uterus at 15 days, mice typically deliver early. Inversely, an SP-A inhibitor injection causes notable delays in birth. The presence of Surfactant Protein A seemed to trigger an inflammatory response in the uterus of the mice, but later studies found an anti-inflammatory response in humans. In fact, the level of ...
Idiopathic Pulmonary Fibrosis (IPF) is a fatal lung disease, histologically characterized by diffuse interstitial remodeling and patchy inflammation. A significant percentage of IPF patients have a familial form of the disease. Separate reports have identified mutations in Surfactant Protein-C (SFTPC), Surfactant Protein-A2 (SFTPA2), Telomerase Reverse Transcriptase (TERT) or Telomerase RNA component (TERC) in these families.. We determined the frequency of mutations in SFTPC, SFTPA2, TERT and TERC in 20 patients with Familial Pulmonary Fibrosis (FPF).. Heterozygous non-tolerated sequence changes were detected in 12 out of 20 patients, consisting of 5 SFTPC, 2 SFTPA2 and 5 TERT mutations. Mutations segregated with disease in each family and haplotype analysis showed that identical mutations had arisen independently. Families with SFTPC and SFTPA2 mutations always had evidence of parent-offspring disease transmission, while in families with TERT mutation sibs were affected. Pediatric pulmonary ...
Principal Investigator:UEDA Takashi, Project Period (FY):1997 - 1998, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:Respiratory organ internal medicine
The pulmonary collectins, surfactant proteins A (SP-A) and D (SP-D), have been reported to bind lipopolysaccharide (LPS), opsonize microorganisms, and enhance the clearance of lung pathogens. In this study, we examined the effect of SP-A and SP-D on the growth and viability of Gram-negative bacteria. The pulmonary clearance of Escherichia coli K12 was reduced in SP-A-null mice and was increased in SP-D-overexpressing mice, compared with strain-matched wild-type controls. Purified SP-A and SP-D inhibited bacterial synthetic functions of several, but not all, strains of E. coli, Klebsiella pneumoniae, and Enterobacter aerogenes. In general, rough E. coli strains were more susceptible than smooth strains, and collectin-mediated growth inhibition was partially blocked by coincubation with rough LPS vesicles. Although both SP-A and SP-D agglutinated E. coli K12 in a calcium-dependent manner, microbial growth inhibition was independent of bacterial aggregation. At least part of the antimicrobial ...
... allows for the in vitro quantitative determination of Bovine Surfactant-associated protein 2, SFTA2 concentrations in serum, plasma, tissue homogenates, cell culture supernates or other biological fluids.
DI-fusion, le Dépôt institutionnel numérique de lULB, est loutil de référencementde la production scientifique de lULB.Linterface de recherche DI-fusion permet de consulter les publications des chercheurs de lULB et les thèses qui y ont été défendues.
Surfactant proteins A (SP-A) and D (SP-D) have been implicated in pulmonary innate immunity. The proteins are host defense lectins, belonging to the collectin family which also... ...
Human innate host defense molecules, surfactant protein A1 (SP-A1), and SP-A2 differentially affect the function and proteome of the alveolar macrophage (AM). We hypothesized that SP-A genes differentially regulate the AM miRNome. Humanized transgenic mice expressing SP-A1 and SP-A2 were subjected to O3-induced oxidative stress (OxS) or filtered air (FA), AMs were isolated, and miRNA levels were measured. In SP-A2 males, we found significant changes in miRNome in terms of sex and sex-OxS effects, with 11 miRNAs differentially expressed under OxS. Their mRNA targets included BCL2, CAT, FOXO1, IL6, NF-kB, SOD2, and STAT3. We followed the expression of these transcripts as well as key cytokines, and we found that (a) the STAT3 mRNA significantly increased at 4 h post OxS and returned to baseline at 18 h post OxS. (b) The anti-oxidant protein SOD2 level significantly increased, but the CAT level did not change after 4 h post OxS compared to control. (c) The anti-apoptotic BCL2 mRNA increased significantly
Recombinant surfactant protein A and pharmaceutical compositions based thereon are useful for the prevention or treatment of pulmonary infection and inflammation.
Klasická cesta aktivace komplementu je spuštěna komplexem C1 (C1q, C1r, C1s), rozpozná-li Fc oblast imunoglobulinu navázaného na povrchový antigen patogena.. C1q nemá C-lektinovou doménu jako SP-A a MBL a není klasifikován jako kolektin. Namísto toho má C1q globulární doménu rozpoznávající Fc oblast imunoglobulinu navázaného na povrchový antigen. Vzhledem k podobnosti primární struktury C1q, SP-A a MBL není překvapivé, že se tyto proteiny podobají také ve své funkci. Všechny tři molekuly hrají roli v přirozené imunitě, např. umocňují fagocytózu mikroorganismů.[7][8] Všechny tři proteiny také vážou stejný C1qR.[9] Bylo prokázáno, že SP-A pomáhá makrofágům odstraňovat neutrofily umírající apoptózou.[10] Tato funkce byla dříve popsána u C1q. Navzdory strukturním podobnostem SP-A či SP-D nemůžou nahradit C1q při klasické aktivaci komplementu.[11]. Součástí obrany proti patogenům v plicích jsou surfaktanty SP-A a SP-D i ...
Surfactant protein A1 (SP-A or SP-A1) is a member of the C-type lectin family of proteins, known as collectins. In humans, it is encoded by the SFTPA1 gene. SP-A is the major protein component of pulmonary surfactant, a lipoprotein complex secreted by the alveolar type II cell. Pulmonary surfactant reduces surface tension in the alveolus and prevents alveolar collapse during exhalation. In addition to its role as a surfactant, SP-A modulates the alveolar immune response to microbes and inhaled particulate matter. SP-A is also expressed in nonalveolar cells, and is thought to be involved in functions such as immune cell proliferation, stimulation of proinflammatory cytokine expression, and control of reactive oxygen species. Mutations in the SFTPA1 gene are associated with idiopathic pulmonary fibrosis. SP-A is also known as alveolar proteinosis protein, 35 kDa pulmonary surfactant-associated protein, pulmonary surfactant-associated protein A1, surfactant protein A1B, collectin-4, SP-A1, PSAP, ...
Surfactant protein A1 (SP-A or SP-A1) is a member of the C-type lectin family of proteins, known as collectins. In humans, it is encoded by the SFTPA1 gene. SP-A is the major protein component of pulmonary surfactant, a lipoprotein complex secreted by the alveolar type II cell. Pulmonary surfactant reduces surface tension in the alveolus and prevents alveolar collapse during exhalation. In addition to its role as a surfactant, SP-A modulates the alveolar immune response to microbes and inhaled particulate matter. SP-A is also expressed in nonalveolar cells, and is thought to be involved in functions such as immune cell proliferation, stimulation of proinflammatory cytokine expression, and control of reactive oxygen species. Mutations in the SFTPA1 gene are associated with idiopathic pulmonary fibrosis. SP-A is also known as alveolar proteinosis protein, 35 kDa pulmonary surfactant-associated protein, pulmonary surfactant-associated protein A1, surfactant protein A1B, collectin-4, SP-A1, PSAP, ...
Surfactant protein D, also known as SFTPD or SP-D, is a protein which in humans is encoded by the SFTPD gene. SFTPD is an innate immune system collectin. Surfactant protein D has been shown to interact with DMBT1, and hemagglutinin of influenza A virus. pulmonary surfactant GRCh38: Ensembl release 89: ENSG00000133661 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000021795 - Ensembl, May 2017 "Human PubMed Reference:". "Mouse PubMed Reference:". Rust K, Grosso L, Zhang V, Chang D, Persson A, Longmore W, Cai GZ, Crouch E (October 1991). "Human surfactant protein D: SP-D contains a C-type lectin carbohydrate recognition domain". Arch. Biochem. Biophys. 290 (1): 116-26. doi:10.1016/0003-9861(91)90597-C. PMID 1898081. Lu J, Willis AC, Reid KB (June 1992). "Purification, characterization and cDNA cloning of human lung surfactant protein D". Biochem. J. 284. 284 ( Pt 3): 795-802. PMC 1132609 . PMID 1339284. "Entrez Gene: SFTPD surfactant, pulmonary-associated protein D". Brandt EB, Mingler ...
Other research interest include; pulmonary surfactant subtype conversion, alterations of pulmonary surfactant in acute respiratory distress syndrome, the use of surfactant supplementation for the treatment of acute respiratory Distress Syndrome and pulmonary surfactant in lung transplantation. Most of these studies are done in collaboration with Drs Lewis, Possmayer and Novick.. Publications. Lewis JF, Veldhuizen RA. The Future of Surfactant Therapy during ALI/ARDS. Semin Respir Crit Care Med. 2006 Aug;27(4):377-88.. Bailey TC, Maruscak AA, Petersen A, White S, Lewis JF, Veldhuizen RA. Physiologic effects of oxidized exogenous surfactant in vivo: effects of high tidal volume and surfactant protein-A. Am J Physiol Lung Cell Mol Physiol. 2006 Apr 21; [Epub ahead of print]. Huang W, McCaig LA, Veldhuizen RA, Yao LJ, Lewis JF. Mechanisms responsible for surfactant changes in sepsis-induced lung injury. Eur Respir J. 2005 Dec;26(6):1074-9.. Da Silva K, McCaig LA, Veldhuizen RA, Possmayer F. Protein ...
Other research interest include; pulmonary surfactant subtype conversion, alterations of pulmonary surfactant in acute respiratory distress syndrome, the use of surfactant supplementation for the treatment of acute respiratory Distress Syndrome and pulmonary surfactant in lung transplantation. Most of these studies are done in collaboration with Drs Lewis, Possmayer and Novick.. Publications. Lewis JF, Veldhuizen RA. The Future of Surfactant Therapy during ALI/ARDS. Semin Respir Crit Care Med. 2006 Aug;27(4):377-88.. Bailey TC, Maruscak AA, Petersen A, White S, Lewis JF, Veldhuizen RA. Physiologic effects of oxidized exogenous surfactant in vivo: effects of high tidal volume and surfactant protein-A. Am J Physiol Lung Cell Mol Physiol. 2006 Apr 21; [Epub ahead of print]. Huang W, McCaig LA, Veldhuizen RA, Yao LJ, Lewis JF. Mechanisms responsible for surfactant changes in sepsis-induced lung injury. Eur Respir J. 2005 Dec;26(6):1074-9.. Da Silva K, McCaig LA, Veldhuizen RA, Possmayer F. Protein ...
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RPB039Hu01, Recombinant Surfactant Associated Protein D (SPD), 表面活性物质关联蛋白D(SPD)重组蛋白, SFTPD; COLEC7; PSP-D; SFTP4; SP-D; Pulmonary Surfactant Protein D; Collectin-7; Lung surfactant protein D | 仅供体外研究使用,不用于临床诊断!请索取进口关税税单及报关单!
Adult hamsters were exposed to 100% oxygen for up to 8 days. At time of death lung tissue was analyzed for the expression of surfactant protein (SP) genes, and surfactant was isolated from alveolar lavage fluid. Surfactant was analyzed for the composition of proteins and phospholipids and for its surface properties. We found, over the 8 days of exposure, that an alveolitis composed of polymorphonuclear leukocytes (PMNs) and alveolar macrophages, accompanied by exudation of edema fluid, appeared in the alveolar spaces. The steady-state levels of SP mRNAs declined after 8 days of exposure to 100% oxygen, but the patterns indicated individual genetic control. SP-A was elevated early in the course of the hyperoxic exposure but decreased significantly by day 8; SP-B decreased continuously; SP-C was unchanged (or slightly elevated) through day 2 and then declined. The amounts of recoverable lavage surfactant increased by greater than threefold, and the phospholipid composition showed increasing percentages of
Surfactant protein D小鼠单克隆抗体[10B2](ab26267)可与人样本反应并经WB, ELISA实验严格验证,被4篇文献引用。所有产品均提供质保服务,中国75%以上现货。
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乙氧基化月见草油甘油酯类 - 表面活性剂 - 表面活性剂百科 - 表面活性剂百科(Surfactant.TOP),表面活性剂,阴离子表面活性剂,阳离子表面活性剂,非离子表面活性剂,两性离子表面活性剂,氟表面活性剂,硅表面活性剂,纯天然表面活性剂,高分子表面活性剂,生物表面活性剂,特殊表面活性剂 - 第1页
棕櫚油醯谷氨酸鈉 - 表面活性劑 - 表面活性劑百科 - 表面活性劑百科(Surfactant.TOP),表面活性劑,陰離子表面活性劑,陽離子表面活性劑,非離子表面活性劑,兩性離子表面活性劑,氟表面活性劑,矽表面活性劑,純天然表面活性劑,高分子表面活性劑,生物表面活性劑,特殊表面活性劑 - 第1頁
Figure S1: Low donor lung SP-A mRNA-level associates with decreased survival. The graph shows the survival curves for recipients of double lung transplant excluding patient with ILD. This ad hoc analysis was to address the possible selection bias that is shown in Table S1 with greater percentage of ILD and single lung transplant in the study cohort. Lung transplant patients that received lung allografts with low levels of SP-A mRNA expression prior to implantation had significantly reduced survival. The number of patients in each group is indicated in brackets. The x-axis represents the cumulative survival. Circles indicate the censored patients within the analysis. ...
Collectins are oligomeric proteins composed of C type lectin domains connected to collagen regions (1). Three collectins are known in humans: mannan-binding lectin (MBL), a serum protein, and the lung surfactant proteins A and D (SP-A and SP-D), which are produced by epithelial cells mainly in the lung. The collectins play an important role in innate immunity by binding to specific carbohydrate structures found on the surfaces of pathogenic microorganisms, including bacteria, viruses, yeasts, and parasitic protozoa. The binding promotes effector mechanisms such as aggregation, hindrance of infection, activation of phagocytes, and initiation of phagocytosis. After binding to microbial surfaces, MBL activates the complement system through a complement activation pathway, the MBL pathway, by using two recently identified serine proteases, MASP-1 and MASP-2, to activate C4 and C2 (2).. SP-D is mainly produced by alveolar type II cells but is also present in sweat, salivary, tear, and mammary glands ...
Pulmonary surfactant is a complex mixture of phospholipids and proteins, which is present in the alveolar lining fluid and is essential for normal lung function. Alterations in surfactant composition have been reported in several interstitial lung diseases (ILDs). Furthermore, a mutation in the surfactant protein C gene that results in complete absence of the protein has been shown to be associated with familial ILD. The role of surfactant in lung disease is therefore drawing increasing attention following the elucidation of the genetic basis underlying its surface expression and the proof of surfactant abnormalities in ILD.
Adaptation to respiration at birth depends upon the synthesis of pulmonary surfactant, a lipid-protein complex that reduces surface tension at the air-liquid interface in the alveoli and prevents lung collapse during the ventilatory cycle. Herein, we demonstrated that the gene encoding a subunit of the endoplasmic reticulum membrane complex, EMC3, also known as TMEM111 (Emc3/Tmem111), was required for murine pulmonary surfactant synthesis and lung function at birth. Conditional deletion of Emc3 in murine embryonic lung epithelial cells disrupted the synthesis and packaging of surfactant lipids and proteins, impaired the formation of lamellar bodies, and induced the unfolded protein response in alveolar type 2 (AT2) cells. EMC3 was essential for the processing and routing of surfactant proteins, SP-B and SP-C, and the biogenesis of the phospholipid transport protein ABCA3. Transcriptomic, lipidomic, and proteomic analyses demonstrated that EMC3 coordinates the assembly of lipids and proteins in ...
Rynkiewicz MJ, Wu H, Cafarella TR, Nikolaidis NM, Head JF, Seaton BA, McCormack FX. (2017) Differential Ligand Binding Specificities of the Pulmonary Collectins Are Determined by the Conformational Freedom of a Surface Loop. Biochemistry. Aug 8; 56(31):4095-4105. PMID: 28719181.. Rynkiewicz MJ, Fischer S, Lehman W. (2016) The propensity for tropomyosin twisting in the presence and absence of F-actin. Arch Biochem Biophys. 2016 Nov 1; 609:51-58. PMID: 27663225.. Goh BC, Wu H, Rynkiewicz MJ, Schulten K, Seaton BA, McCormack FX. (2016) Elucidation of Lipid Binding Sites on Lung Surfactant Protein A Using X-ray Crystallography, Mutagenesis, and Molecular Dynamics Simulations. Biochemistry. 2016 Jul 5; 55(26):3692-701. PMID: 27324153.. Fischer S, Rynkiewicz MJ, Moore JR, Lehman W. (2016) Tropomyosin diffusion over actin subunits facilitates thin filament assembly. Struct Dyn. 2016 Jan 14; 3(1):012002. PMID: 26798831.. Rynkiewicz MJ, Schott V, Orzechowski M, Lehman W, Fischer S. (2015) Electrostatic ...
Biotin偶联Surfactant protein D抗体[IIE11](ab15695)可与大鼠, 人样本反应并经WB, IHC实验严格验证,被2篇文献引用,实验条件参看说明书。中国75%以上现货。
Metastasis is a major cause of cancer-related deaths. A dearth in preclinical models that recapitulates the metastatic microenvironment has impeded the development of therapeutic agents that are effective against metastatic disease. Since the majority of solid tumors metastasize to the lung, we developed a multi-cellular lung organoid that mimics the lung microenvironment with air sac like structures and production of lung surfactant protein. We used these cultures called primitive lung-in-a-dish (PLiD), to recreate metastatic disease using primary and established cancer cells. The metastatic tumor-in-a-dish (mTiD) cultures resemble the architecture of metastatic tumors in the lung including angiogenesis. Pretreating PLiD with tumor exosomes enhanced cancer cell colonization. We next tested the response of primary and established cancer cells to current chemotherapeutic agents and an anti-VEGF antibody in mTiD against cancer cells in 2-dimensional (2D) or 3D cultures. The response of primary ...
surfactant chemistry manufacturers surfactant chemistry suppliers Directory - Browse surfactant chemistry products,Choose Quality surfactant chemistry manufacturers, suppliers, factory at B2BAGE
What is Surfactant? The alveoli contain many types of cells. Among them Type 2 Pneumocytes produces surfactant. The main function of surfactant is to reduce surface tension, so that decrease the work of breathing. Surfactant forms a thin monomolecular layer at the air fluid interface. Surfactant layer is not static. It is continuously secreting and reabsorbing. Deficiency of surfactant causes Respiratory …. Read More » ...
Surfactant, substance such as a detergent that, when added to a liquid, reduces its surface tension, thereby increasing its spreading and wetting properties. In the dyeing of textiles, surfactants help the dye penetrate the fabric evenly. Learn more about surfactants in this article.
表面張力素(Surfactant)在懷孕20週已經出現3隨著週數增加到了28週-30週醫生就能在羊水中測到它的成分》而胎兒荷爾蒙中的TSH就是在18-20過時急速上升3連帶也帶動了T4》從20-30過快速上升3這或許是表面張力素開始製造的訊息》30-32週胎兒的腎上腺素功能加強3類固醇荷爾蒙快速上升3帶動Surfactant中的PC(Phosphatidylcholine)與S(Sphingomyelin)一起上升3而在35過時PC大量製造3但S卻製造減少3取代的卻是PG(Phosphatidylglycerol)的快速出現且製造增加3這時也觀察到類固醇荷爾蒙量正是最多的時候》簡言之18-30週受TSH T4》荷爾蒙影響較大330-35週受類固醇荷爾蒙影響較強3而真正轉捋點是在35週那個時候3一方面PC(構造性)大量製造3一方面PG(功能性)突然的出現 ...
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Looking for online definition of Pulmonary surfactant-associated protein a in the Medical Dictionary? Pulmonary surfactant-associated protein a explanation free. What is Pulmonary surfactant-associated protein a? Meaning of Pulmonary surfactant-associated protein a medical term. What does Pulmonary surfactant-associated protein a mean?
Lung surfactant reduces surface tension and maintains the stability of alveoli. How surfactant is released from alveolar epithelial type II cells is not fully understood. Vacuolar ATPase (V-ATPase) is the enzyme responsible for pumping H+ into lamellar bodies and is required for the processing of surfactant proteins and the packaging of surfactant lipids. However, its role in lung surfactant secretion is unknown. Proteomic analysis revealed that vacuolar ATPase (V-ATPase) dominated the alveolar type II cell lipid raft proteome. Western blotting confirmed the association of V-ATPase a1 and B1/2 subunits with lipid rafts and their enrichment in lamellar bodies. The dissipation of lamellar body pH gradient by Bafilomycin A1 (Baf A1), an inhibitor of V-ATPase, increased surfactant secretion. Baf A1-stimulated secretion was blocked by the intracellular Ca2+ chelator, BAPTA-AM, the protein kinase C (PKC) inhibitor, staurosporine, and the Ca2+/calmodulin-dependent protein kinase II (CaMKII), KN-62. Baf A1
Pulmonary surfactant proteins and lipids are required for lung function after birth. Lung immaturity and resultant surfactant deficiency cause respiratory distress syndrome, a common disorder contributing to morbidity and mortality in preterm infants. Surfactant synthesis increases prior to birth in association with formation of the alveoli that mediate efficient gas exchange. To identify mechanisms controlling perinatal lung maturation, the Calcineurin b1 (Cnb1) gene was deleted in the respiratory epithelium of the fetal mouse. Deletion of Cnb1 caused respiratory failure after birth and inhibited the structural maturation of the peripheral lung. Synthesis of surfactant and a lamellar body-associated protein, ABC transporter A3 (ABCA3), was decreased prior to birth. Nuclear factor of activated T cells (Nfat) calcineurin-dependent 3 (Nfatc3), a transcription factor modulated by calcineurin, was identified as a direct activator of Sftpa, Sftpb, Sftpc, Abca3, Foxa1, and Foxa2 genes. The ...
Toda la información sobre las últimas publicaciones científicas de la Clínica Universidad de Navarra. Surfactant protein d, a marker of lung innate immunity, is positively associated with insulin sensitivity
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Adaptation to respiration at birth depends upon the synthesis of pulmonary surfactant, a lipid-protein complex that reduces surface tension at the air-liquid interface in the alveoli and prevents lung collapse during the ventilatory cycle. Herein, we demonstrated that the gene encoding a subunit of the endoplasmic reticulum membrane complex, EMC3, also known as TMEM111 (Emc3/Tmem111), was required for murine pulmonary surfactant synthesis and lung function at birth. Conditional deletion of Emc3 in murine embryonic lung epithelial cells disrupted the synthesis and packaging of surfactant lipids and proteins, impaired the formation of lamellar bodies, and induced the unfolded protein response in alveolar type 2 (AT2) cells ...
Receptor (or element of a larger receptor complex) for C1q, mannose-binding lectin (MBL2) and pulmonary surfactant protein A (SPA). May mediate the enhancement of phagocytosis in monocytes and macrophages upon interaction with soluble defense collagens. May play a role in intercellular adhesion.
AT-100 is a protein replacement therapy targeting Bronchopulmonary Dysplasia. AT-100 is a recombinant form of human surfactant protein-D (rhSP-D). SP-D performs 3 critical roles in maintaining healthy lung fuction.
A mild, multi-phase cleansing composition is described that includes a cleansing phase including a structured surfactant component has a first density; a benefit phase includes an emulsion, the benefi