YTHDF2 Knockout HCT 116 Cell Line

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YTHDF2 Knockout HCT 116 Cell Line
Cat.No.:

EDC07749

Species:

Human

Cell Name:

HCT 116

Gene:

YTHDF2

Gene ID:

51441

Size:

1×10⁶cells

YTHDF2 Knockout HCT116 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. EDC07749
Product Name YTHDF2 Knockout HCT116 Cell Line
Species Human
Cell Line HCT 116
Cellosaurus ID CVCL_0291
Gene ID
Cell Line Synonyms HCT-116, HCT.116, HCT_116, HCT116, HCT116wt, HCT-116/P, HCT-116/parental, CoCL2
Gene YTHDF2
Gene Synonyms CAHL|DF2|HGRG8|NY-REN-2
Summary
This gene encodes a member of the YTH (YT521-B homology) superfamily containing YTH domain. The YTH domain is typical for the eukaryotes and is particularly abundant in plants. The YTH domain is usually located in the middle of the protein sequence and may function in binding to RNA. In addition to a YTH domain, this protein has a proline rich region which may be involved in signal transduction. An Alu-rich domain has been identified in one of the introns of this gene, which is thought to be associated with human longevity. In addition, reciprocal translocations between this gene and the Runx1 (AML1) gene on chromosome 21 has been observed in patients with acute myeloid leukemia. This gene was initially mapped to chromosome 14, which was later turned out to be a pseudogene. Alternatively spliced transcript variants encoding different isoforms have been identified in this gene. [provided by RefSeq, Oct 2012]
Associated Diseases Colorectal Carcinoma
Digestion Time 3 min
Morphology Adherent
Passage Ratio 1:4~1:5
Complete Culture Medium mcCoy5A+10% FBS
Freezing Medium 90% FBS/complete culture medium+10% DMSO
* 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: HCT 116		STR Info (Cell bank)
Cell Line: HCT 116
Allele1Allele2Allele3Allele4Allele1Allele2Allele3Allele4
Amelogenin X X
CSF1PO 7 10 7 9 10 11
D2S1338 16 16
D3S1358 12 17 18 19 12 18 19
D5S818 10 11 10 11
D7S820 11 12 11 12
D8S1179 10 12 14 15 10 12 14 15
D13S317 10 12 10 12
D16S539 11 13 11 12 13 14
D18S51 16 17 16 17
D19S433 12 13 12
D21S11 29 30 29 30
FGA 18 23 18 23
Penta D 9 13 9 13
Penta E 12 13 14 12 13 14
TH01 8 9 8 9
TPOX 8 8
vWA 17 21 22 23 17 21 22 23
D6S1043 13
D12S391 17 21 22
D2S441 11 12
* 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 asking what m6A-marked transcripts depend on YTHDF2-mediated decay, or whether forced YTHDF2 expression is sufficient to accelerate the degradation of candidate transcripts. The Knockout line reveals which transcripts stabilize when YTHDF2 is absent — the central question in YTHDF2 biology. Overexpression is more useful for testing sufficiency or for dissecting paralog competition with YTHDF1 and YTHDF3. For m6A-mediated decay research, the EDITGENE Knockout line is generally the more informative tool because YTHDF family proteins have overlapping functions, and overexpression of one paralog can be confounded by displacement of others. Rescue with wild-type or m6A-binding-defective (W432A) YTHDF2 is the standard specificity control for assigning phenotypes to m6A reader activity.
Primary applications: • MeRIP-seq + RNA-seq: comparing m6A modification landscapes and steady-state transcript levels between knockout and wild-type cells to identify YTHDF2-regulated transcripts; direct targets require orthogonal half-life validation. • mRNA stability assays: actinomycin D chase for candidate m6A-modified transcripts to confirm YTHDF2-dependent decay. • Cancer phenotype assays: proliferation, apoptosis sensitivity, and metabolic pathway activity readouts relevant to colorectal cancer biology. • Pathway studies: investigation of YTHDF2-regulated programs in cell cycle control, DNA damage response, and stress adaptation. EDITGENE recommends this model for researchers investigating m6A epitranscriptomics, mRNA decay mechanisms, and colorectal cancer-relevant gene regulation.
Yes. YTHDF2 rescue experiments have a well-established specificity control framework due to the maturity of m6A reader research: • Construct design: use a codon-modified YTHDF2 sequence with a C-terminal tag (FLAG, HA). Both N- and C-terminal tags are generally tolerated for YTH family proteins. • m6A-binding-defective rescue: the W432A mutation in the YTH domain abolishes m6A binding and is the standard specificity control for assigning phenotypes to m6A reader activity. Rescue with wild-type but not W432A YTHDF2 confirms m6A-dependent function. • Paralog considerations: YTHDF1 and YTHDF3 share substantial sequence similarity and overlapping target transcripts with YTHDF2. If studying transcript-specific effects, consider whether observed phenotypes might reflect paralog redundancy rather than YTHDF2-specific function. • Functional readout: rescue should restore m6A-modified transcript decay rates (measured by mRNA half-life assays for candidate targets) and accompanying phenotypic outputs in HCT 116. HCT 116 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=2.9
International reviews of immunology
Inflammation induces tumor formation and plays a crucial role in tumor progression and prognosis. KCNK6, by regulating K(+) efflux to reduce NLRP3 Inflammasome-induced lung injury, relaxes the aorta. This study aims to elucidate the effects and biological mechanism of KCNK6 in inflammation-associated carcinogenesis, which may be essential for colon homeostasis and the defense system. To induce colitis, mice were given 3.0% Dextran Sodium Sulfate (DSS) in their drinking water for 7 days. The Azoxymethane (AOM) +DSS method was used to induce colon cancer in the mice model. Bone marrow-derived macrophages (BMDM) from Kcnk6-/- mice, AW264.7 cells, and human colon cancer HCT116 and Caco2 cells were used as models. The loss of Kcnk6 prevented spontaneous colitis and restored mucosal integrity and homeostatic molecules. Additionally, the loss of Kcnk6 reduced the severity of AOM/DSS-induced carcinogenesis. Kcnk6 promoted cell viability and proliferation in HCT-116 or Caco-2 cells. The loss of Kcnk6 inhibited the levels of inflammatory factors in BMDM cells. Kcnk6 accelerated potassium channel activity, inducing NLRP3 inflammasome activation. METTL3-mediated m6A modification increased Kcnk6 stability in a YTHDF2-dependent manner. Histone lactylation activated the transcription of YTHDF2/Kcnk6. Our study revealed the important role of Kcnk6 in inflammation-associated carcinogenesis progression. The m6A methyltransferase METTL3 and histone lactylation increased Kcnk6 stability in a YTHDF2-dependent manner, providing a potential strategy for inflammation-associated carcinogenesis or colorectal cancer therapy.

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