PVRIG Knockout HEK293 Cell Line

PVRIG Knockout HEK293 Cell Line
Cat.No.:

EDC07584

Species:

Human

Cell Name:

HEK293

Gene:

PVRIG

Gene ID:

79037

Size:

1×10⁶cells

PVRIG Knockout Cell Line (HEK293) is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performance Cas9 Protein and Hassle-Free Cell Selection.
Cat.No. EDC07584
Product Name PVRIG Knockout Cell Line (HEK 293)
Cell Line HEK293
Cellosaurus ID CVCL_0045
Cell Line Synonyms Hek293, HEK-293, HEK/293, (HEK)293, HEK 293, HEK,293, 293, 293 HEK, 293 Ad5, Graham 293, Graham-293, Human Embryonic Kidney 293
Gene PVRIG
NCBI Gene ID
Gene Synonyms C7orf15|CD112R
Summary
Enables phosphatase binding activity and signaling receptor activity. Involved in negative regulation of T cell receptor signaling pathway. Located in plasma membrane. [provided by Alliance of Genome Resources, Jul 2025]
Associated Diseases Non-tumor
Morphology Adherent
Passage Ratio 1/5,2days
Complete Culture Medium DMEM + 10% FBS
Freezing Medium 95% Complete culture medium+ 5% DMSO
QC Indels validated by Sanger sequencing; sterility confirmed via microbial testing.
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.
LociSTR Info (Sample Cell)
Sample Cell Line: HEK293
STR Info (Cell bank)
Cell Line: HEK293
Allele1Allele2Allele1Allele2
Amelogenin X X
CSF1P0 12 11 12
D2S1338 19 19
D3S1358 15 17 15 17
D5S818 8 8 9
D7S820 11 12 11 12
D8S1179 12 14 12 14
D13S317 12 14 12 14
D16S539 9 13 9 13
D18S51 17 18 17 18
D19S433 15 18 15 18
D21S11 28 30.2 28 30.2
FGA 23 23
Penta D 9 10 9 10
Penta E 7 15 7 15
TH01 7 9.3 7 9.3
TPOX 11 11
vWA 16 19 16 19
D6S1043 11 11
D12S391 19 21 11 15
D2S441 11 15 11 15
* STR authentication data of this cell line matches with that of cell lines sourced from ATCC, DSMZ, JCRB, and RIKEN databases.
Conclusion: The STR identification of this cell is correct.

FAQ

The choice depends on whether you are studying PVRIG (CD112R)'s role as an emerging immune checkpoint receptor or its interactions with the PVR family (CD155, CD112, TIGIT, CD96, CD226). The Knockout line is the standard tool for asking whether PVRIG is required for inhibitory signaling on T cells and NK cells — PVRIG binds CD112 (PVRL2/nectin-2) and competes with CD226 (DNAM-1), forming an inhibitory pair analogous to TIGIT-CD155. Overexpression is useful for studying PVRIG signaling or for testing receptor-ligand binding. Important consideration: PVRIG is principally expressed on T cells and NK cells — HEK293 is not the physiological context for PVRIG function. The EDITGENE Knockout in HEK293 is most useful for biochemical and antibody specificity validation work. It serves as a critical negative control for anti-PVRIG antibodies in development as cancer immunotherapy agents (COM701/nelistotug and others). For physiological PVRIG immune signaling research, T cell or NK cell models are more appropriate. Rescue with wild-type or signaling-deficient PVRIG enables structure-function studies.
Primary applications: • Anti-PVRIG antibody validation: critical genetic specificity control for anti-PVRIG/CD112R antibodies including COM701 (nelistotug) in clinical development as cancer immunotherapy. • CD112 (PVRL2) binding: in vitro binding assays for PVRIG-CD112 interaction in the absence of endogenous PVRIG. • PVR family receptor studies: PVRIG-CD226 (DNAM-1) competition for CD112 binding, analogous to TIGIT-CD226 competition for CD155. • Heterologous PVRIG expression: structure-function and biochemical studies of PVRIG variants. EDITGENE recommends this model for researchers in cancer immunotherapy antibody development and PVR family receptor biochemistry. Physiological PVRIG inhibitory signaling research requires T cell or NK cell models.
Yes. PVRIG rescue experiments are well-established for immune checkpoint research: • Construct design: use a codon-modified PVRIG sequence with a small intracellular C-terminal tag (FLAG, HA). PVRIG is a type I membrane protein with an N-terminal Ig-V domain (CD112 binding) and intracellular ITIM/ITT-like motifs — preserve all elements. • Surface localization validation: confirm plasma membrane localization by cell surface staining before functional assays. • Signaling-deficient rescue: cytoplasmic tail ITIM/ITT-like motif mutations enable separation of ligand binding from intracellular inhibitory signaling. • Functional readout: rescue should restore CD112 binding (flow cytometry) and antibody recognition for antibody specificity validation. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.

Required Accessories

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