SCGB1A1

Case Study 1: Ruixi Zhou, 2019

Sepsis has a high in clinic neonatal mortality. Moreover, a considerable number of children's brains remain affected even after the treatment of sepsis and it often leaves sequelae. Therefore, early intervention for sepsis is of considerable significance. Recent studies have shown that Club cell protein (CC16) is closely related to the p38 mitogen-activated protein kinase (MAPK) signaling pathway, which can regulate inflammation, oxidative stress, apoptosis, and autophagy during sepsis. Thus, the researchers analyzed the neuroprotective effect of recombinant CC16 (rCC16) in a neonatal sepsis rat model. For the first time, they found that the p38MAPK signaling pathway was activated in neonatal brain tissue of rats with sepsis, and the CC16 levels decreased significantly. Secondly, after the rCC16 interference, the occurrence of inflammation, oxidative stress and apoptosis were subsequently reversed, and autophagy was further stimulated. Finally, through further intervention using the p38MAPK signaling pathway inhibitor, SB203580, or its agonist, anisomycin, they confirmed that rCC16 reduced rat mortality and improve general conditions. Simultaneously, it had also neuroprotective effect. Its mechanism could be related to oxidative stress, inflammation, and apoptosis reduced and autophagy activated by rCC16 inhibiting the p38MAPK signaling pathway.

Fig1. Vital signs at 12 h after operation for each group.

Fig2. Effect of rCC16 treatment on the pathological changes in CLP rats at 12 h.

Case Study 2: Min Pang, 2015

Clara cell protein (CC16) is a well-known anti-inflammatory protein secreted by the epithelial Clara cells of the airways. Previous studies suggest that CC16 gene transfer suppresses expression of interleukin (IL)-8 in bronchial epithelial cells. However, its role in the function of these cells during inflammation is not well understood. This study evaluated the effect of CC16 on the expression of matrix metalloproteinase (MMP)-9 in lipopolysaccharide (LPS)-stimulated rat tracheal epithelial cells and its underlying molecular mechanisms. The researchers generated recombinant rat CC16 protein (rCC16) which was bioactive in inhibiting the activity of phospholipase A2. rCC16 inhibited LPS-induced MMP-9 expression at both mRNA and protein levels in a concentration-dependent (0-2 μg/mL) manner, as demonstrated by real time RT-PCR, ELISA, and zymography assays. Gene transcription and DNA binding studies demonstrated that rCC16 suppressed LPS-induced NF-κB activation and its binding of gene promoters as identified by luciferase reporter and gel mobility shift assays, respectively. Western blotting and immunofluorescence staining analyses further revealed that rCC16 concentration dependently inhibited the effects of LPS on nuclear increase and cytosol reduction of NF-κB, on the phosphorylation and reduction of NF-κB inhibitory IκBα, and on p38 MAPK-dependent NF-κB activation by phosphorylation at Ser276 of its p65 subunit.

Fig3. Acid–base titration analysis shows concentration-dependent inhibition of PLA2 activity by rCC16.

Fig4. rCC16 inhibits LPS-induced phosphorylation of IκBα in RTE cells.

SCGB1A1 involved in several pathways and played different roles in them. We selected most pathways SCGB1A1 participated on our site, such as , which may be useful for your reference. Also, other proteins which involved in the same pathway with SCGB1A1 were listed below. Creative BioMart supplied nearly all the proteins listed, you can search them on our site.

SCGB1A1 has several biochemical functions, for example, . Some of the functions are cooperated with other proteins, some of the functions could acted by SCGB1A1 itself. We selected most functions SCGB1A1 had, and list some proteins which have the same functions with SCGB1A1. You can find most of the proteins on our site.

SCGB1A1 has direct interactions with proteins and molecules. Those interactions were detected by several methods such as yeast two hybrid, co-IP, pull-down and so on. We selected proteins and molecules interacted with SCGB1A1 here. Most of them are supplied by our site. Hope this information will be useful for your research of SCGB1A1.