WFS1 Knockout HEK293 Cell Line

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WFS1 Knockout HEK293 Cell Line
Cat.No.:

EDC07862

Species:

Human

Cell Name:

HEK293

Gene:

WFS1

Gene ID:

7466

Size:

1×10⁶cells

WFS1 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. EDC07862
Product Name WFS1 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 WFS1
NCBI Gene ID
Gene Synonyms CTRCT41|WFRS|WFS|WFSL
Summary
This gene encodes a transmembrane protein, which is located primarily in the endoplasmic reticulum and ubiquitously expressed with highest levels in brain, pancreas, heart, and insulinoma beta-cell lines. Mutations in this gene are associated with Wolfram syndrome, also called DIDMOAD (Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy, and Deafness), an autosomal recessive disorder. The disease affects the brain and central nervous system. Mutations in this gene can also cause autosomal dominant deafness 6 (DFNA6), also known as DFNA14 or DFNA38. Alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Mar 2009]
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 WFS1's role in ER homeostasis and the unfolded protein response, or modeling Wolfram syndrome-associated phenotypes. The Knockout line is the standard tool for both — Wolfram syndrome is caused by loss-of-function WFS1 mutations, so KO recapitulates the genetic basis of disease. Overexpression is more useful for testing whether elevated WFS1 is sufficient to suppress ER stress, or for studying WFS1's interactions with calcium homeostasis machinery. For ER stress and Wolfram syndrome modeling, the EDITGENE Knockout line in HEK293 is the more disease-relevant model. Rescue with wild-type or Wolfram syndrome-associated mutant WFS1 (e.g., specific missense variants) is particularly informative for genotype-phenotype correlation studies.
Primary applications: • ER stress response: XBP1 splicing, ATF4/CHOP induction, and BiP expression following tunicamycin or thapsigargin treatment to assess UPR activation in WFS1-deficient cells. • Calcium homeostasis: ER calcium store measurements using Fura-2 or genetically encoded calcium sensors. • Beta cell relevance studies: insulin processing and secretion assays if pancreatic beta cell biology is the focus (though HEK293 is not a beta cell model). • Wolfram syndrome modeling: rescue with disease-associated WFS1 mutations to study genotype-phenotype relationships. EDITGENE recommends this model for researchers investigating ER homeostasis, unfolded protein response, and Wolfram syndrome mechanisms.
Yes. WFS1 rescue experiments require attention to ER membrane targeting and Wolfram syndrome mutation analysis: • Construct design: use a codon-modified WFS1 sequence. WFS1 is a multi-pass ER membrane protein — C-terminal tags are strongly preferred, and signal sequence/topology must be preserved. • Localization validation: confirm ER membrane localization of exogenous WFS1 by immunofluorescence co-staining with calnexin or PDI before functional assays. • Wolfram syndrome mutation rescue: disease-associated missense variants can be introduced for genotype-phenotype correlation studies in a controlled background. • Functional readout: rescue should restore baseline UPR markers (XBP1 splicing, BiP, CHOP) and ER calcium homeostasis to wild-type levels. HEK293 transduces efficiently with lentivirus and supports both polyclonal and clonal rescue line generation.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.

Related Publications

IF=15.7
Nature communications
The sorting of soluble secretory proteins from the endoplasmic reticulum (ER) to the Golgi complex is mediated by coat protein complex II (COPII) vesicles and thought to required specific ER membrane cargo-receptor proteins. However, these receptors remain largely unknown. Herein, we show that ER to Golgi transfer of vesicular cargo proteins requires WFS1, an ER-associated membrane protein whose loss of function leads to Wolfram syndrome. Mechanistically, WFS1 directly binds to vesicular cargo proteins including proinsulin via its ER luminal C-terminal segment, whereas pathogenic mutations within this region disrupt the interaction. The specific ER export signal encoded in the cytosolic N-terminal segment of WFS1 is recognized by the COPII subunit SEC24, generating mature COPII vesicles that traffic to the Golgi complex. WFS1 deficiency leads to abnormal accumulation of proinsulin in the ER, impeding the proinsulin processing as well as insulin secretion. This work identifies a vesicular cargo receptor for ER export and suggests that impaired peptide hormone transport underlies diabetes resulting from pathogenic WFS1 mutations.
This KO model may be useful for: - Studying ER-to-Golgi vesicular transport and cargo protein export mechanisms - Investigating endoplasmic reticulum (ER) stress and unfolded protein response (UPR) pathways - Modeling pancreatic β-cell dysfunction and diabetes-related pathology - Evaluating the role of WFS1 in protein trafficking and secretion assays - Screening compounds targeting ER homeostasis and cellular stress responses

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