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Vitamin B12 test kit

LipoKnoxa™ Human BBS7 shRNA Ad5 Particle (Silencing)

Cat. No.: V0126XX53
Species: Human
Target Gene: BBS7
Vector System: Adenovirus
Modulation Type: Silencing (shRNA)
LipoKnoxa™ Human BBS7 shRNA Ad5 Particle (Silencing)
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Sub Cat. No. TargetSeq Region Inquiry
V0126XX53-1 GCAGGAGAATGTGTGACATTT CDS Inquiry
V0126XX53-2 ATGAATCAGTTGACAACAAAT 3' UTR Inquiry
V0126XX53-3 GAAATCGTGGTGTCCACATAT CDS Inquiry
V0126XX53-4 Other Inquiry

Product Overview

Description: LipoKnoxa™ Human BBS7 shRNA Ad5 Particle (Silencing) provides an efficient method to silence BBS7, a core component of the BBSome complex required for ciliary membrane protein trafficking. Deficiency in BBS7 is a known cause of Bardet-Biedl syndrome, which manifests with central obesity. Through high-efficiency Ad5 delivery of optimized shRNA (U6 or miR30), researchers can investigate ciliary signaling disruptions. We ensure experimental safety and data integrity through comprehensive QC, including functional titer measurement and negative results for sterility and mycoplasma.
Production Cell Line: HEK293
Viral Backbone: Adenovirus type 5 (dE1/E3)
Promoter: U6; CMV; EF1α; CAG; UBC
Product Availability: Produced Upon Order

Specification

Titer Test: qPCR
Insert Verification: All viral preparations are validated via Sequencing and PCR to ensure 100% sequence identity and the structural integrity of the vector genomes.
Sterility Test: This product has been certified sterile following comprehensive microbial growth analysis, confirming the absence of bacterial and fungal contamination.
Mycoplasma Test: This product was certified negative for mycoplasma contamination following stringent QC analysis, ensuring the absence of all mycoplasmal agents.
Other QC: Beyond standard protocols, we offer customized knockdown efficiency validation through in vitro and in vivo assessments. This includes precise analysis of mRNA/protein reduction and subsequent biological responses to ensure the functional potency of the shRNA-mediated gene silencing.
Storage: Upon receipt, viral preparations should be immediately transferred to -80°C for long-term storage to ensure maximum stability and maintain product integrity.
Stability: This product maintains excellent biological activity for 6–12 months (and up to 2 years in specific cases) when stored continuously at -80°C. Once thawed, the working solution remains stable for 2–3 weeks at 4°C without significant loss of viral potency.
Shipping Condition: All viral preparations are shipped on dry ice to ensure maximum biological activity and stability during transit.
Handling Notes: Viral particles are susceptible to temperature fluctuations and freeze-thaw cycles. To preserve functional titers, it is essential to aliquot the vector into low-protein-binding tubes immediately upon first thaw. To ensure experimental success and biological safety, all procedures must be conducted within a certified biosafety cabinet.
Intended Use: This product is intended for research use only and is not for use in diagnosis or therapeutic applications.
Product Disclaimer: While our products are committed to excellence through rigorous internal QC inspections, we cannot guarantee specific performance or experimental outcomes due to the inherent complexity of biological systems. Users assume full responsibility for product storage, handling, and strict compliance with all applicable safety protocols, biosafety requirements, and legal regulations during all operational processes.

Target Profile

Gene Name: BBS7
Full Name: Bardet-Biedl syndrome 7
Gene Symbol: BBS2L1
Gene ID: 55212
RefSeq ID-1: NP_060660.2
RefSeq ID-2: NM_018190.3
Summary: BBS7 encodes a core component of the BBSome complex, an eight-protein assembly essential for primary cilium formation and function. The BBSome facilitates Rab8-mediated trafficking of signaling receptors to cilia, thereby regulating ciliogenesis. Assembly of the BBSome requires chaperonin-like BBS proteins and CCT/TRiC chaperonins. Mutations in BBS7 are associated with Bardet–Biedl syndrome, a ciliopathy characterized by obesity, retinal degeneration, polydactyly, and renal abnormalities. Two transcript variants encoding distinct isoforms have been reported.
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