Human GNAS ELISA Kit

Background Pigmentation development, is a complex process regulated by many transcription factors during development. With the development of the RNA sequencing (RNA-seq), non-coding RNAs, such as miRNAs, lncRNAs, and circRNAs, are found to play an important role in the function detection of related regulation factors. In this study, we provided the expression profiles and development of ncRNAs related to melanocyte and skin development in mice with black coat color skin and mice with white coat color skin during embryonic day 15 (E15) and postnatal day 7 (P7). The expression profiles of different ncRNAs were detected via RNA-seq and also confirmed by the quantitative real-time PCR (qRT-PCR) method. GO and KEGG used to analyze the function the related target genes. Results We identified an extensive catalogue of 206 and 183 differently expressed miRNAs, 600 and 800 differently expressed lncRNAs, and 50 and 54 differently expressed circRNAs, respectively. GO terms and pathway analysis showed the target genes of differentially expressed miRNA and lncRNA. The host genes of circRNA were mainly enriched in cellular process, single organism process. The target genes of miRNAs were mainly enriched in chromatin binding and calcium ion binding in the nucleus. The function of genes related to lncRNAs are post translation modification. The competing endogenous RNA (ceRNA) network of lncRNAs and circRNAs displays a complex interaction between ncRNA and mRNA related to skin development, such as Tcf4, Gnas, and Gpnms related to melanocyte development. Conclusions The ceRNA network of lncRNA and circRNA displays a complex interaction between ncRNA and mRNA related to skin development and melanocyte development. The embryonic and postnatal development of skin provide a reference for further studies on the development mechanisms of ncRNA during pigmentation.

GNAS mutations have been described in mucinous and non-mucinous epithelial neoplasms of the appendix, pancreas, and colon, with hotspot GNAS mutations found in up to two-thirds of pancreatic intraductal papillary mucinous neoplasms. Additionally, many GNAS-mutated tumors have concurrent mutations in the Ras/Raf pathway. The clinicopathologic features of GNAS-mutated lung carcinomas, however, have not yet been characterized. Primary lung carcinomas from Brigham and Women's Hospital (n=1282) or Massachusetts General Hospital (n=1070) were genotyped on a targeted massively parallel sequencing panel of oncogenes and tumor suppressor genes including GNAS. Clinical and pathological features were reviewed, and TTF-1 immunohistochemistry was performed when material was available. Nineteen lung adenocarcinomas with hotspot GNAS mutations were identified (19/2352, 0.8%) including 14 at codon 201 and 5 at codon 227. GNAS-mutated lung adenocarcinomas occurred predominantly in female patients (16/19, 84%). Ten (10) were classified as invasive mucinous adenocarcinomas (IMA), and nine (9) were non-mucinous adenocarcinomas. All IMAs had GNAS codon 201 mutations and concurrent Ras/Raf pathway mutations (9 KRAS, 1 BRAF). No tumors with GNAS codon 227 mutations had mucinous histological features. 86% of GNAS-mutated non-mucinous adenocarcinomas (6/7) were positive for TTF-1 immunohistochemistry, while only 25% of GNAS-mutated IMAs (1/4) were positive for TTF-1. Patients with GNAS-mutated non-mucinous adenocarcinomas were more likely to have a history of smoking (9/9, 100%) compared to patients with GNAS-mutated IMAs (2/10, 20%) (P < 0.001). Hotspot GNAS mutations can occur in primary lung adenocarcinomas. When associated with concurrent mutations in the Ras/Raf pathway, these neoplasms often present as IMAs. GNAS mutations are not specific to neoplasms of the gastrointestinal tract, and clinicopathologic correlation is necessary in GNAS-mutated adenocarcinomas in the lung to determine the primary site of origin.