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SCGB1A1 encodes a member of the secretoglobin family of small secreted proteins.
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Our data suggest that rCC16 suppresses LPS-mediated inflammatory mediator TNF-alpha (Montrer TNF Kits ELISA), IL-6 (Montrer IL6 Kits ELISA), and IL-8 (Montrer IL8 Kits ELISA) production by inactivating NF-kappaB (Montrer NFKB1 Kits ELISA) and p38 MAPK (Montrer MAPK14 Kits ELISA) but not AP-1 (Montrer FOSB Kits ELISA) in RAW264.7 cells.
Lung-specific (CC-16) and novel (RelB (Montrer RELB Kits ELISA)) biomarkers are associated with systemic cardiovascular changes over time. CC-16 can predict subsequent exacerbations in subjects with severe COPD (Montrer ARCN1 Kits ELISA) and may be an important biomarker of pulmonary and systemic stress in COPD (Montrer ARCN1 Kits ELISA).
Smokers and COPD patients had reduced airway CC16 immunostaining that decreased with in (Montrer NFKB1 Kits ELISA)creasing COPD severity.
the uteroglobin G38A gene polymorphism was not associated with IgAN risk
In chromium-exposed workers, blood levels of CC16, and CC16/SP-D (Montrer SFTPD Kits ELISA) were lower than in controls. Positive relationships were shown between CC16 or CC16/SP-D (Montrer SFTPD Kits ELISA) and indicators of lung function.
Increased plasma clara cell secretory protein levels are associated with primary graft dysfunction.
Uteroglobin is a possible ligand of the lipoxin receptor and it may have a role in inhibiting serum amyloid A-driven inflammation
This study extends the function of the Scgb1a1-expressing epithelial cell population as a major mediator of the antiviral response. It
CC16 protects lungs from cigarette smoke (CS)-induced injury by reducing lung NF-kappaB (Montrer NFKB1 Kits ELISA) activation. CS-induced airway CC16 deficiency increases CS-induced pulmonary inflammation and injury and likely contributes to the pathogenesis of COPD (Montrer ARCN1 Kits ELISA).
Suggest role for Scgb1a1(+) cells in the generation of p63 (Montrer CKAP4 Kits ELISA)(+) cells in the damaged lung parenchyma.
Serum CC-16 is associated with disease progression in chronic obstructive pulmonary disease (COPD (Montrer ARCN1 Kits ELISA)). However, the absence of CC-16 does not appear to modify the risk of cigarette-related COPD (Montrer ARCN1 Kits ELISA) in mice.
the role of clara cells and clara cell secretory protein in lung radiation injury exacerbated by viral infection
AAV2/9-CC10 vector virus guaranteed sufficient CC10 expression and had an anti-inflammatory effect in asthmatic mice.
Claudin-3 (Montrer CLDN3 Kits ELISA) and Clara cell 10 kDa protein were identified as possible markers of early tobacco smoke-induced epithelial injury along alveolar ducts.
Scgb1a1-expressing cells, most likely Clara cells, are a major cell type that gives rise to alveolar type I and II cells during the regeneration of alveolar epithelia in response to severe pulmonary damage in mice.
These results indicate that CC10 gene transfer may inhibit airway inflammation through suppressing the activation of NF-kappaB (Montrer NFKB1 Kits ELISA).
Clara cell secretory protein expression is elevtaed in lungs after long-term n-hexane inhalation exposure.
This gene encodes a member of the secretoglobin family of small secreted proteins. The encoded protein has been implicated in numerous functions including anti-inflammation, inhibition of phospholipase A2 and the sequestering of hydrophobic ligands. Defects in this gene are associated with a susceptibility to asthma.
, clara cell phospholipid-binding protein
, clara cells 10 kDa secretory protein
, urinary protein 1
, urine protein 1
, PCB-binding protein
, clara cell 17 kDa protein
, clara cell secretory protein
, secretoglobin family 1A member 1
, Uteroglobin (Clara cell secretory protein)