BPI Fold Containing Family A, Member 1 Proteine (BPIFA1)

Human BPI Fold Containing Family A, Member 1 (BPIFA1) Interaktionspartner

1. data indicate that SPLUNC1 is an allosteric regulator of ENaC that dissociates alphabetagamma-ENaC to generate a new SPLUNC1-beta-ENaC complex.

2. Study proposes that BPIFA1 (SPLUNC1) is the epithelium-derived smooth muscle relaxing factor and it functions by internalizing Orai1. BPIFA1 deficiency in asthmatic airways promotes Orai1 hyperactivity, increased airway smooth muscle contraction and airway hyperresponsiveness.

3. BPIFA1 and BPIFB1 expressions are correlated with goblet cell metaplasia and inversely correlated with lung function parameters of airway obstruction (FEV1 and FEV1/FVC) in COPD patients.

4. SPLUNC1 has antimicrobial and antibiofilm activities against the Burkholderia cepacia complex.

5. Data show that the palate, lung, and nasal epithelium clone (PLUNC) protein level was highly expressed in nontumor nasopharyngeal epithelium than that in nasopharyngeal carcinoma (NPC) tissues.

6. These studies identify the role of SPLUNC1 in sinonasal innate immunity and the pathogenesis of CRS. Defective expression of SPLUNC1 in CRSwNP patients may lead to insufficient maintenance of the epithelial barrier function

7. High serum SPLUNC1 levels are associated with Pleural Effusion from Lung Cancer Compared to Tuberculosis.

8. PLUNC is a protein of the tear film and suggest that it plays a role in fluid balance and surface tension regulation at the ocular surface.

9. SPLUNC1 can weaken the inflammatory response induced by EBV infection in NPC cells through the regulation of the TLR9/NF-kappaB signaling pathway and control of the tumor inflammatory microenvironment

10. The G allele of rs1078761 may be detrimental to lung function in cystic fibrosis owing to decreased levels of BPIFA1 and BPIFB1.

11. LUNX silencing disrupted primary tumor growth, local invasion, and metastatic colonization

12. pleural fluid LUNX mRNA provided a valuable adjunct in distinguishing malignant pleural effusion caused by lung cancer from benign pleural effusion

13. The observations suggest that, in response to agents or chemical factors, nasal mucosal epithelium will react and produce PLUNC proteins

14. discoveries provide insight into the specific determinants governing the interaction between SPLUNC1 and lipids and also shed light on novel functions that SPLUNC1 and other PLUNC family members perform in host defense

15. 12 retinoid X receptors heterodimer binding sites exist in the SPLUNC1 promoter region, which is up-regulated by all-trans-retinoic acid. SPLUNC1 plays a role in ATRA-induced growth inhibition and differentiation in nasopharyngeal carcinoma cells.

16. Our results indicate that BPIFA1 is a novel target for autoantibodies in cystic fibrosis.

17. The correlation between SPLUNC1 levels and Vol2(increase) in non-smokers may indicate involvement of SPLUNC1in the regulation of the normal function of the nasal mucosa.

18. In patients with chronic rhinosinusitis with nasal polyps, decreased PLUNC expression is associated with multibacterial colonization, specifically those mediated by Staphyloccocus aureus and Pseudomonas aeruginosa.

19. BPIFA1 protein displays bacteriocidal activity against Gram-negative bacteria.

20. SPLUNC1 is differentially modulated in eosinophilic and noneosinophilic chronic rhinosinusitis with nasal polyps.

Pig (Porcine) BPI Fold Containing Family A, Member 1 (BPIFA1) Interaktionspartner

1. High expression level in trachea and lung tissue only

Mouse (Murine) BPI Fold Containing Family A, Member 1 (BPIFA1) Interaktionspartner

1. Bpifa1-deficient (Bpifa1-/-) mice exhibited spontaneous airway hyperresponsiveness and that excised tracheas from Bpifa1+/+ but not Bpifa1-/- mice were capable of reducing airway smooth muscle contraction.

2. this study shows that BPIFA1/SPLUNC1 restricts influenza A virus infection

3. SPLUNC1-knockout mice was established in a LPS-induced acute lung injury (ALI) mouse model to study the anti-inflammatory effect of SPLUNC1. Results found that SPLUNC1 deficiency upregulated levels of ALI-related cytokines leading to more severe lung injury after LPS injection. Moreover, further data discovered that the presence of SPLUNC1 can suppress the recruitment of CD11b+Gr-1+ MDSCs to the spleen in LPS-induced ALI.

4. Loss of Splunc1 predisposes mice to the development of otitis media.

5. SPLUNC1 is a crucial component of mucosal innate immune defense against pulmonary infection.

6. Knowledge of the complex expression patterns of BPIF proteins in these regions will allow the use of tractable mouse models of disease to dissect their function.

7. SPLUNC1 is present at high concentrations in murine airways under basal conditions, whereas it is suppressed by low-level environmental pathogen-associated molecular patterns and inflammatory signals.

8. SPLUNC1 KO mice demonstrated significantly higher numbers of eosinophils in the lung after OVA challenges than did wild-type mice.

9. Our findings demonstrate a critical in vivo role of SPLUNC1 in host defense against bacterial infection

10. Our data for the first time suggest that airway epithelial TLR2 signaling is pivotal in mycoplasma-induced SPLUNC1 production.

11. splunc5, splunc1, and lplunc1 are expressed in unique domains along a continuous corridor of oral, lingual, pharyngeal, and respiratory epithelia

12. SPLUNC1 protein decreases Mycoplasma pneumoniae (Mp) levels and inhibits epithelial IL-8 production induced by Mp-derived lipoproteins.