HEK293 HBS1L-HibiT Knock In Cell Line

HEK293 HBS1L-HibiT Knock In Cell Line

Item	Cat#	Price
Stable Cell Line	SNB-H-0003A	Inquiry
Compound Test Services	CT-001	$1,950 per 384w plate *(Up To 16 cpds Dose)*

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Product Description

HBS1L (HBS1-like translational GTPase) is a GTPase that, together with Pelota, rescues stalled ribosomes to maintain translational fidelity. It also participates in the no‑go decay (NGD) pathway of mRNA surveillance. Synthetic lethality between the PELO–HBS1L and SKI complexes has been identified in cancers with FOCAD deletion or SKI complex destabilization, positioning HBS1L as a promising therapeutic target for these tumors.

ScreeningBio's HEK293 HBS1L-HibiT Knock In Cell Line enables quantitative measurement of target protein levels in a single assay. In this system, the HiBiT-tagged HBS1L expressed from the endogenous locus complements with exogenously added LgBiT to generate a luminescent signal directly proportional to the amount of HBS1L present, allowing accurate and reproducible quantification of HBS1L degradation.

Product Specifications

Target Type	Translational GTPases
Species	Human
HGNC Symbol	HBS1L
Accession Number	NM_006620.4
Parental Line	HEK293
Lot#	See Vial
Storage	Liquid Nitrogen

Data

HEK293 HBS1L-HibiT Knock In Assay. HEK293 HBS1L-HibiT Knock In cells were treated with the TNG961. Non-linear regression was used to plot activity changes vs. [Compound, M] and DC50 values were determined using GraphPad Prism software. — **HEK293 HBS1L-HibiT Knock In Assay.** HEK293 HBS1L-HibiT Knock In cells were treated with the TNG961. Non-linear regression was used to plot activity changes vs. [Compound, M] and DC₅₀ values were determined using GraphPad Prism software.

**HEK293 HBS1L-HibiT Knock In Assay Sanger Sequencing Results.**

Target Background

HBS1L (HBS1-like translational GTPase) is a GTPase that, together with Pelota, rescues stalled ribosomes to maintain translational fidelity. It also participates in the no‑go decay (NGD) pathway of mRNA surveillance.

Synthetic lethality between the PELO–HBS1L and SKI complexes has been identified in cancers with FOCAD deletion or SKI complex destabilization, positioning HBS1L as a promising therapeutic target for these tumors.