AMBRA1 Knockout HEK293 Cell Line

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AMBRA1 Knockout HEK293 Cell Line
Cat.No.:

EDC07527

Species:

Human

Cell Name:

HEK293

Gene:

AMBRA1

Gene ID:

55626

Size:

1×10⁶cells

AMBRA1 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. EDC07527
Product Name AMBRA1 Knockout Cell Line (HEK293)
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 AMBRA1
NCBI Gene ID
Gene Synonyms DCAF3|WDR94
Summary
Enables enzyme binding activity; protein phosphatase activator activity; and ubiquitin-like ligase-substrate adaptor activity. Involved in several processes, including macroautophagy; positive regulation of free ubiquitin chain polymerization; and positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transduction. Located in cytosol. Part of Cul4-RING E3 ubiquitin ligase complex. Is active in cytoskeleton; mitochondrion; and nucleus. Biomarker of multiple system atrophy. [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 AMBRA1's recently characterized role as a Cyclin D1 ubiquitin ligase substrate receptor or modeling autophagy and emerging cancer applications. The Knockout line is the standard tool for asking whether AMBRA1 is required for these processes — AMBRA1 was originally characterized as a Beclin-1-interacting autophagy regulator; landmark 2021 studies (three concurrent Nature papers: Maiani et al., Simoneschi et al., Chaikovsky et al.) identified AMBRA1 as the long-sought Cyclin D1 substrate receptor of a Cullin-4 E3 ligase (CRL4^AMBRA1) that targets D-type cyclins for degradation; AMBRA1 is therefore a tumor suppressor restraining D-cyclin-CDK4/6 activity. Overexpression is useful for studying AMBRA1 gain-of-function effects. For cancer biology research, the EDITGENE AMBRA1 Knockout in HEK293 is uniquely valuable — AMBRA1 is one of the most important newly characterized cancer drug targets, with potential to extend CDK4/6 inhibitor sensitivity through preventing D-cyclin degradation. Rescue with wild-type AMBRA1 enables structure-function studies of both the Cyclin D1-degrading and autophagy-regulating functions. The knockout is valuable for studying Cullin-4 substrate receptor biology, D-cyclin regulation, CDK4/6 inhibitor sensitivity, and emerging AMBRA1-targeted approaches — this is one of the most clinically promising recent discoveries in cell cycle biology.
Primary applications: • Cyclin D1 stability: D-type cyclin (CCND1, CCND2, CCND3) protein half-life analysis (cycloheximide chase) in AMBRA1-null cells. • CRL4^AMBRA1 substrate identification: ubiquitinome analysis to characterize AMBRA1 substrates. • CDK4/6 inhibitor sensitivity: in heterologous breast cancer-relevant contexts, AMBRA1 loss may confer altered CDK4/6 inhibitor (palbociclib/ribociclib/abemaciclib) sensitivity. • Autophagy regulation: Beclin-1 interaction and autophagy initiation analysis. EDITGENE recommends this model for researchers investigating Cyclin D1 regulation, CDK4/6 inhibitor sensitivity, and emerging AMBRA1-related cancer therapeutic strategies — a major recent discovery (2021 Nature triple-papers).
Yes. AMBRA1 rescue experiments are uniquely powerful for the dual-function biology: • Construct design: use a codon-modified AMBRA1 sequence with a small C-terminal tag (FLAG, HA). AMBRA1 has multiple WD40 repeats and DDB1-binding region — preserve all elements. • Cyclin D1-binding-deficient rescue: substrate-binding region mutations affect D-cyclin recognition. • DDB1-binding-deficient rescue: DDB1-binding region mutations affect CRL4 complex assembly. • Beclin-1-binding rescue: Beclin-1-interaction region mutations separate autophagy from Cyclin D1-ligase functions. • Functional readout: rescue should restore D-cyclin degradation kinetics and autophagy initiation. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation for systematic AMBRA1 functional dissection.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.

Related Publications

IF=48.5
Nature
D-type cyclins are central regulators of the cell division cycle and are among the most frequently deregulated therapeutic targets in human cancer, but the mechanisms that regulate their turnover are still being debated. Here, by combining biochemical and genetics studies in somatic cells, we identify CRL4 (also known as CRL4) as the ubiquitin ligase that targets all three D-type cyclins for degradation. During development, loss of Ambra1 induces the accumulation of D-type cyclins and retinoblastoma (RB) hyperphosphorylation and hyperproliferation, and results in defects of the nervous system that are reduced by treating pregnant mice with the FDA-approved CDK4 and CDK6 (CDK4/6) inhibitor abemaciclib. Moreover, AMBRA1 acts as a tumour suppressor in mouse models and low AMBRA1 mRNA levels are predictive of poor survival in cancer patients. Cancer hotspot mutations in D-type cyclins abrogate their binding to AMBRA1 and induce their stabilization. Finally, a whole-genome, CRISPR-Cas9 screen identified AMBRA1 as a regulator of the response to CDK4/6 inhibition. Loss of AMBRA1 reduces sensitivity to CDK4/6 inhibitors by promoting the formation of complexes of D-type cyclins with CDK2. Collectively, our results reveal the molecular mechanism that controls the stability of D-type cyclins during cell-cycle progression, in development and in human cancer, and implicate AMBRA1 as a critical regulator of the RB pathway.
This KO model may be useful for: - Investigating the role of AMBRA1 in CRL4-mediated regulation of D-type cyclins - Cell cycle control and G1/S transition studies - Functional analysis of ubiquitin ligase pathways in proliferation - Mechanistic studies on cyclin D stability and degradation - Cancer research targeting cell cycle checkpoint mechanisms

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