Secretoglobin, Family 3A, Member 1 Proteins (SCGB3A1)

Human Secretoglobin, Family 3A, Member 1 (SCGB3A1) interaction partners

1. Some single nucleotide polymorphisms and their combinations in the Ugrp2 gene are associated with an increased risk of developing adenoid hypertrophy.

2. The role of high in normal-1 (HIN-1) as a potential biomarker in combating glioblastoma is being described for the first time in this study.

3. Tumor-adjacent tissues showed higher methylation status of RASSF1A, HIN-1 and MGMT promoters.

4. SCGB3A1-183 T and SCGB3A1 IVS1-189 A alleles might have a protective effect against nasal polyposis.

5. aberrant HIN-1 promoter methylation could be an independent and important biomarker used in predicting the prognosis and progression of breast cancer

6. Methylation of HIN-1 promoter is a novel epigenetic biomarker associated with poor outcomes in OCCA patients.

7. Methylation of HIN-1, RASSF1A, RIL and CDH13 in breast cancers was associated with clinical characteristics, but only RASSF1A methylation was associated with time to first recurrence and overall survival.

8. HIN1, was the most "dietary sensitive" genes, as methylation of their promoters was associated with intakes of at least two out of the eight dietary methyl factors examined.

9. analysis of AKT signaling pathway activated by HIN-1 methylation in non-small cell lung cancer

10. Data show that SCGB3A1 was down-regulated in invasive compared with DCIS, whereas talin 2 (TLN2) and PTGS1 were up-regulated in invasive compared with DCIS.

11. Data suggest that high methylation of the HIN-1 promoter results in silenced HIN-1 expression in gastric cancer, and that 5-aza-2'-deoxycytidine reverses HIN-1 methylation and reduces viability of gastric cancer cells.

12. The methylation levels and frequencies of HIN1, RASSF1A and TWIST, and average MR were significantly lower in basal-like subtype compared to luminal or human epithelial growth factor receptor-2 subtype.

13. Hypermethylation of HIN-1 is associated with lymphatic metastasis of breast cancers.

14. HIN-1, RAR-beta, RASSF1A, and Twist had the ability to distinguish high-grade squamous intraepithelial lesions/squamous cell carcinomas from low-grade squamous intraepithelial lesions/negative cervical scrapings

15. Sporadic breast tumors with a "BRCA1-like" histopathological phenotype also demonstrated significantly lower frequency of HIN-1 promoter methylation.

16. hypermethylated in invasive and in in situ lobular breast cancer

17. Lack of HIN-1 methylation defines specific breast tumor subtypes including medullary carcinoma of the breast and BRCA1-linked tumors

18. high in normal-1 (HIN-1) is downregulated in stage I non-small cell lung cancer

19. silencing of HIN-1 expression and methylation of its promoter occurs in multiple human cancer types, suggesting that elimination of HIN-1 function may contribute to several forms of epithelial tumorigenesis

20. Aberrant methylation of HIN-1 is a frequent event in many human malignancies

Mouse (Murine) Secretoglobin, Family 3A, Member 1 (SCGB3A1) interaction partners

1. Neonatal hyperoxia followed by RA recovery was associated with decreased lung CCSP and SCGB3A1 protein but not mRNA expression.

2. The differential expression of mRNA by both airway level and lung region was determined for uteroglobin-related protein 2.

3. Highest HIN-1 and UGRP-1 expression is detected in the lung, while lower level HIN-1 expression is also detected in the stomach, heart, small intestine, uterine and mammary glands

4. genomic structure and expression patterns of Ugrp2 and its alternative spliced form were characterized

5. EGF-induced increase of Ugrp2 occurred at the transcriptional level that required the EGF receptor and the activation of the ERK-MAPK and phosphoinositide-3 kinase pathways

6. ubiquitous transcription factor NF-Y binds to and activates expression of the Scgb3a1 gene and tissue-specific expression of the gene is associated with CpG methylation of the promoter

7. The expression of SCGB3A1 and SCGB3A2 are bidirectionally regulated by oncostatin M (OSM) when examined in a mouse transformed Clara cell line.

8. Expression of SCGB3A1 was down-regulated by IFN-gamma in a time- and dose-dependent manner in the murine transformed Clara Cells line.