COPS6 Knockout HAP1 Cell Line

COPS6 Knockout HAP1 Cell Line
Cat.No.:

EDC08259

Species:

Human

Cell Name:

HAP1

Gene:

COPS6

Gene ID:

10980

Size:

1×10⁶cells

COPS6 Knockout HAP1 Cell Line is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performotion Cas9 Protein and Hassle-Free Cell Selection.
Cat.No. EDC08259
Product Name COPS6 Knockout HAP1 Cell Line
Species Human
Cell Line HAP1
Cellosaurus ID CVCL_0F62
Gene ID
Cell Line Synonyms Highly Aggressively Proliferating Immortalized
Gene COPS6
Summary
The protein encoded by this gene is one of the eight subunits of COP9 signalosome, a highly conserved protein complex that functions as an important regulator in multiple signaling pathways. The structure and function of COP9 signalosome is similar to that of the 19S regulatory particle of 26S proteasome. COP9 signalosome has been shown to interact with SCF-type E3 ubiquitin ligases and act as a positive regulator of E3 ubiquitin ligases. This protein belongs to translation initiation factor 3 (eIF3) superfamily. It is involved in the regulation of cell cycle and likely to be a cellular cofactor for HIV-1 accessory gene product Vpr. [provided by RefSeq, Jul 2008]
Digestion Time 2 min
Morphology Adherent
Passage Ratio 1:8~1:10
Complete Culture Medium IMDM+10%FBS
Freezing Medium 90%FBS+10%DMSO
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.

FAQ

The choice depends on whether you are studying COPS6 (CSN6, COP9 signalosome subunit 6)'s role as a component of the COP9 signalosome or modeling its emerging functions in cancer biology. The Knockout line is the standard tool for asking whether COPS6 is required for these processes — COPS6 is one of eight subunits of the COP9 signalosome (CSN, CSN1-8 plus accessory subunits), a multi-protein complex with MPN+/JAMM metalloprotease activity (provided by CSN5/COPS5) that deneddylates cullin-RING ligases (CRLs), regulating CRL E3 ligase activity dynamics. COPS6/CSN6 has been characterized as a cancer-relevant CSN component with overexpression in multiple cancers. Overexpression is useful for studying COPS6 in heterologous expression contexts. For ubiquitin biology research, the EDITGENE COPS6 Knockout in HAP1 enables study of CSN-mediated CRL deneddylation. Rescue with wild-type COPS6 is the standard specificity control. The knockout is valuable for studying CRL E3 ligase regulation, MYC/AKT stability (COPS6 has been implicated in regulating MYC and AKT levels in cancer), and emerging CSN-targeted cancer therapeutics.
Primary applications: • COP9 signalosome assembly: CSN complex assembly and CSN5/COPS5-dependent CRL deneddylation analysis in COPS6-null cells. • Cullin neddylation status: NEDD8-conjugated cullin (CUL1-NEDD8, CUL3-NEDD8, etc.) Western blot analysis given CSN's deneddylation activity. • MYC and AKT stability: protein stability and abundance analysis given COPS6's reported role in regulating these oncogenes. • Cancer biology: in heterologous cancer-relevant contexts, characterization of COPS6's emerging cancer roles. EDITGENE recommends this model for researchers investigating COP9 signalosome biology and emerging COPS6-related cancer biology.
Yes. COPS6 rescue experiments require attention to CSN complex assembly: • Construct design: use a codon-modified COPS6 sequence with a small C-terminal tag (FLAG, HA). COPS6 has the canonical MPN domain architecture — preserve protein integrity. • CSN complex partnership: COPS6 requires other CSN subunits for stable complex assembly — rescue interpretation considers CSN1-8 expression. • Functional readout: rescue should restore CRL deneddylation activity measured by CUL-NEDD8 vs CUL ratio. HAP1-specific considerations: • Diploidization: HAP1 cells gradually diploidize during extended culture — confirm ploidy by flow cytometry at the time of phenotypic assay. • Integration site sensitivity: position effects on transgene expression are more pronounced in near-haploid backgrounds; generating multiple independent rescue clones is strongly recommended. • Transduction efficiency: HAP1 transduces with lentivirus at moderate efficiency — increase MOI compared to standard immortalized lines.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.

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