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AdipoUpX™ Human GNAS Lentiviral Particle (Overexpression)
Cat. No.:
V1225XX421
Species:
Human
Target Gene:
GNAS
Vector System:
Lentiviral
Modulation Type:
Overexpression
SPECIFIC INQUIRY
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Product Overview
Description:
AdipoUpX™ Human GNAS Lentiviral Particle (Overexpression) is a ready-to-use, high-titer vector particle professionally engineered for the stable overexpression of the human GNAS gene. As a complex locus mediating G-protein signaling, its stable integration into the host genome is essential for researching imprinting disorders and their impact on metabolic rate. Every batch undergoes rigorous quality control, including titer, sterility, and mycoplasma testing, to ensure experimental reproducibility and safety. Our modular vector system allows for high flexibility in selecting promoters and markers for precise cellular modeling.
Production Cell Line:
HEK293T
Promoter:
Ubi; CMV; EF1a; Others
Product Availability:
Produced Upon Order
Specification
Titer Test:
qPCR
Insert Verification:
PCR analysis was performed to verify the complete genomic sequence of all viral vector preparations.
Sterility Test:
This product was certified sterile following successful microbial growth analysis.
Mycoplasma Test:
The production quality control confirmed the absence of any mycoplasmal agents.
Other QC:
This comprehensive process includes customized supplementary testing alongside in vitro and in vivo transduction assessments to elucidate transgene expression and functionality.
Storage:
To maintain product integrity, immediate transfer of the vector to a -80 °C is essential following its receipt.
Stability:
Continuous storage at -80°C ensures excellent long-term stability for 6-12 months. Once thawed, the product's working solution should be refrigerated at 4°C and used within 2-3 weeks.
Shipping Condition:
Our lentivirus viral products are shipped using dry ice.
Handling Notes:
Ensure all operations are performed within a biosafety cabinet; upon receiving the vector, immediately aliquot it into low-protein-binding tubes and store according to specified conditions, thus avoiding the titer loss caused by sensitivity to temperature fluctuations and freeze-thaw cycles.
Intended Use:
This product is intended for research use only and is not for use in diagnosis or therapeutic applications.
Product Disclaimer:
Given the diversity and complexity of experimental conditions, we do not guarantee product performance or experimental results in any specific application, despite our company's commitment to product quality and the rigorous internal QC inspections all products have undergone. Ultimate responsibility remains with the user for all operational processes, including storage, handling, and compliance with safety and biosafety protocols.
Target Profile
Gene Name:
GNAS
Full Name:
GNAS complex locus
Gene Symbol:
AHO; GSA; GSP; POH; GPSA; NESP; SCG6; SgVI; GNAS1; PITA3; AIMAH1; C20orf45
Gene ID:
2778
RefSeq ID-1:
NP_001070958.1
RefSeq ID-2:
NM_001077490.3
Summary:
GNAS is a highly complex imprinted locus that produces multiple transcripts expressed maternally, paternally, or biallelically. These transcripts arise from four alternative promoters and 5' exons, with some containing differentially methylated regions (DMRs) that influence gene expression. The locus also generates antisense noncoding RNAs, which may regulate imprinting, and one transcript includes an overlapping open reading frame encoding the unrelated protein Alex. Alternative splicing produces various forms of the stimulatory G-protein alpha subunit, a key mediator linking receptor-ligand interactions to adenylyl cyclase activation and downstream signaling. Multiple transcript variants encoding different isoforms have been identified. Mutations or imprinting defects in GNAS are linked to disorders such as pseudohypoparathyroidism types 1a/1b, Albright hereditary osteodystrophy, McCune-Albright syndrome, progressive osseous heteroplasia, polyostotic fibrous dysplasia, and some pituitary tumors. Importantly, defects in GNAS have also been associated with early-onset monogenic obesity, likely due to disrupted G-protein signaling in hypothalamic pathways that regulate energy balance and fat metabolism.
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