Ask about this productRelated genes to: GNAS antibody
- Gene:
- GNAS NIH gene
- Name:
- GNAS complex locus
- Previous symbol:
- GNAS1
- Synonyms:
- NESP55, NESP, GNASXL, GPSA, SCG6, SgVI
- Chromosome:
- 20q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-29
- Date modifiied:
- 2016-10-05
- Gene:
- GNAS-AS1 NIH gene
- Name:
- GNAS antisense RNA 1
- Previous symbol:
- GNASAS, GNAS-AS
- Synonyms:
- SANG, NESP-AS, NESPAS, GNAS1AS, NCRNA00075
- Chromosome:
- 20q13.32
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2008-06-20
- Date modifiied:
- 2019-04-23
Related products to: GNAS antibody
Related articles to: GNAS antibody
- Non-coding RNAs (ncRNAs) are increasingly recognized as important factors in the progression of schizophrenia (SZ); however, their involvement in disease etiology remains incompletely understood. This study aimed to characterize the genomic architecture of selected SZ-associated regions by examining the co-location of ncRNA and protein-coding genes and to explore sequence variants within these regions for potential associations with clinical outcomes. - Source: PubMed
Publication date: 2026/06/22
Hrovatin KarinKunej TanjaTrampuž Sara RedenšekTerzić TeaPlesničar Blanka KoresGoričar KatjaDolžan Vita - The GNAS locus produces multiple transcripts, including the maternally derived, GNAS-H, and GNAS-NESP55 and the paternally derived GNAS-XL, GNAS-A/B, and GNAS-AS, all of which are expressed in specific tissues. GNAS-Gsα is biparentally expressed in most tissues and imprinted in several tissues, specifically, the proximal tubules, thyroid, gonads, and pituitary. These imprinted transcripts are regulated by five differentially methylated regions (GNAS-DMRs), and hypomethylation in the GNAS-A/B:TSS-DMR causes resistance to hormones, including parathyroid hormone, leading to pseudohypoparathyroidism type 1B (PHP1B). Sporadic PHP1B shows broad methylation defects in the GNAS-DMRs, whereas most familial PHP1B cases show localized methylation defects at the GNAS-A/B:TSS-DMR and GNAS-AS2:TSS-DMR. We identified an inherited maternal exon H variant that causes a GNAS methylation pattern typically observed in sporadic PHP1B. - Source: PubMed
Publication date: 2026/03/16
Urakawa TatsukiHuang HaipengNagai TakuhitoHattori AtsushiKawasaki TomoyukiSaitsu HirotomoAkutsu HidenoriFukami MakiKagami Masayo - Osteoarthritis (OA) is a debilitating joint disease affecting over 500 million people globally, characterized by cartilage degradation, chronic pain, and failed tissue repair. Neurogenic inflammation, driven by neuropeptides including Substance P (SP) and calcitonin gene-related peptide (CGRP), plays a key role in the pathogenesis of OA. This study explores the therapeutic potential of extracellular vesicles (EVs) derived from infrapatellar fat pad mesenchymal stem/stromal cells (IFP-MSCs) transduced with CGRP antagonist CGRP (aCGRP IFP-MSC EVs). These EVs are enriched in anti-inflammatory miRNAs and proteins, and they express neprilysin (CD10), enabling SP degradation. Herein, several LncRNAs were identified, which have been known to interact with miRNAs that affect the knee joint homeostasis. Specifically, 11 LncRNAs (ZFAS1, EMX2OS, HOTAIRM1, RPS6KA2-AS1, DANCR, LINC-ROR, GACAT1, GNAS-AS1, HAR1A, OIP5-AS1, TERC) interact with miRNAs that promote cell proliferation, prevent apoptosis, and preserve homeostasis. In vitro, aCGRP IFP-MSC EVs downregulated pro-inflammatory markers (TNF, TLR4, MAPK8) in dorsal root ganglia and promoted chondrocyte gene expression consistent with anabolism and matrix remodeling. In vivo, intra-articular EV delivery attenuated pain behaviors, preserved the cartilage structure, restored PRG4+ stem/progenitor cell localization, and trended toward reduced SP levels. Histological analysis confirmed improved collagen organization and reduced matrix degradation. These findings suggest that aCGRP IFP-MSC EVs exert multimodal effects on neuroinflammation, cartilage regeneration, and joint homeostasis. This cell-free, gene-enhanced EV therapy offers a promising disease-modifying strategy for the treatment of OA, with the potential to address both structural changes and chronic pain associated with this disease. - Source: PubMed
Publication date: 2025/12/09
Liebmann KevinCastillo MarioJergova StanislavaRahimi BehnazKaplan Lee DBest Thomas MSagen JacquelineKouroupis Dimitrios - Natural killer (NK) cells, a key component of the innate immune system, play a crucial role in detecting and eliminating cancer cells, contributing to cancer immune surveillance. Increasing evidence suggests that NK cell functions are regulated by epigenetic mechanisms, including the influence of long non-coding RNAs (lncRNAs). These lncRNAs, transcripts longer than 200 nucleotides, are emerging as important regulators of gene expression. In this study, we investigated the expression of 84 lncRNAs in NK cells isolated from the peripheral blood of patients with invasive breast cancer. Using lncRNA PCR array profiling, we identified 26 differentially expressed lncRNAs in circulating NK cells isolated from peripheral blood of breast cancer patients, with 10 genes showing significant downregulation and 16 genes showing significant upregulation. Gene ontology (GO) and functional enrichment analysis revealed that among the ten downregulated lncRNAs, four lncRNAs have deposited gene ontology terms and known biological functions. These lncRNAs are PTENP1-AS (fold change 0.27, P = 0.0206), TSIX (fold change 0.05, P = 0.0037), XIST (fold change 0.42, P = 0.007), and CCAT1 (fold change 0.09, P = 0.0191). On the other hand, among the 16 upregulated lncRNAs, five lncRNAs have deposited gene ontology terms and known biological functions. These lncRNAs are GNAS-AS1 (fold change 5.10, P = 0.0104), MEG3 (fold change 46.85, P = 0.0138), CDKN2B-AS1 (fold change 81.80, P = 0.0087), HOTAIR (fold change 6.86, P = 0.0042), and AIRN (fold change 7.97, P = 0.0379). Functional enrichment analysis indicated that the downregulated lncRNAs were mainly involved in biological processes such as chromatin organization, epigenetic regulation of gene expression, and dosage compensation via X chromosome inactivation, while the upregulated lncRNAs were linked to epigenetic regulation, genomic imprinting, and chromatin remodeling. These enrichments were identified using Bonferroni correction with an adjusted P-value < 0.05. Given the biological functions of the dysregulated lncRNAs in NK cells from breast cancer patients, this has the potential to significantly impact the antitumor functionality of NK cells, possibly contributing to the impaired immune surveillance and tumor control commonly observed in breast cancer patients. Understanding the dysregulation of lncRNAs in NK cells may provide critical insights into the mechanisms underlying impaired NK cell function in breast cancer, offering promising approaches for developing immunotherapies aiming at restoring NK cell activity in cancer patients. - Source: PubMed
Publication date: 2025/08/09
Rady MonaMohamed EmanKhorshid OlaAbou-Aisha Khaled - LncRNAs interact with miRNAs and mRNAs that can have a special expression pattern in a specific cell type. We investigated the specific lncRNAs, miRNAs, and mRNAs in different groups of prostate cancer (PC). - Source: PubMed
Publication date: 2025/01/26
Vahabzadeh GelarehPashapour-Yeganeh AmirrezaEini MaryamRoudbaraki MoradEsmati EbrahimPoorkhani AmirhoushangKhalighfard SolmazAlizadeh Ali Mohammad