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NDUFS3 KO cell line available to order. KO validated by Western blot. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, Homozygous: 19 bp deletion in exon 1.

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Images

Western blot - Human NDUFS3 knockout HEK-293T cell line (AB266419), expandable thumbnail
  • Western blot - Human NDUFS3 knockout HEK-293T cell line (AB266419), expandable thumbnail
  • Western blot - Human NDUFS3 knockout HEK-293T cell line (AB266419), expandable thumbnail
  • Western blot - Human NDUFS3 knockout HEK-293T cell line (AB266419), expandable thumbnail
  • Sanger Sequencing - Human NDUFS3 knockout HEK-293T cell line (AB266419), expandable thumbnail

Key facts

Cell type
HEK-293T
Species or organism
Human
Tissue
Kidney
Form
Liquid
Knockout validation
Sanger Sequencing, Western blot
Mutation description
Knockout achieved by using CRISPR/Cas9, Homozygous: 19 bp deletion in exon 1

Alternative names

CI 30, CI-30kD, COMPLEX I, MITOCHONDRIAL RESPIRATORY CHAIN, 30-KD SUBUNIT, Complex I 30kDa subunit, Complex I-30kD, NADH coenzyme Q reductase, NADH dehydrogenase (ubiquinone) Fe S protein 3 30kDa, NADH dehydrogenase [ubiquinone] iron sulfur protein 3 mitochondrial, NADH dehydrogenase [ubiquinone] iron-sulfur protein 3, NADH dehydrogenase ubiquinone 30 kDa subunit, NADH-Ubiquinone Oxidoreductase Fe-S Protein 3, NADH-ubiquinone oxidoreductase 30 kDa subunit, NDUS3_HUMAN, mitochondrial

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NDUFS3 KO cell line available to order. KO validated by Western blot. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, Homozygous: 19 bp deletion in exon 1.

Key facts

Cell type
HEK-293T
Form
Liquid
Mutation description
Knockout achieved by using CRISPR/Cas9, Homozygous: 19 bp deletion in exon 1
Concentration
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Properties

Gene name
NDUFS3
Gene editing type
Knockout
Gene editing method
CRISPR technology
Knockout validation
Sanger Sequencing, Western blot
Zygosity
Homozygous

Quality control

STR analysis
CSF1PO, D13S317, D7S820, D5S818, TH01, D16S539, TPOX

Cell culture

Biosafety level
EU: 2 US: 2
Adherent/suspension
Adherent
Gender
Female

Handling procedures

Initial handling guidelines

Upon arrival, the vial should be stored in liquid nitrogen vapor phase and not at -80°C. Storage at -80°C may result in loss of viability.

1. Thaw the vial in 37°C water bath for approximately 1-2 minutes.
2. Transfer the cell suspension (0.8 mL) to a 15 mL/50 mL conical sterile polypropylene centrifuge tube containing 8.4 mL pre-warmed culture medium, wash vial with an additional 0.8 mL culture medium (total volume 10 mL) to collect remaining cells, and centrifuge at 201 x g (rcf) for 5 minutes at room temperature. 10 mL represents minimum recommended dilution. 20 mL represents maximum recommended dilution.
3. Resuspend the cell pellet in 5 mL pre-warmed culture medium and count using a haemocytometer or alternative cell counting method seed all remaining cells into a T25.
4. Incubate the culture at 37°C incubator with 5% CO2. Check the culture one day after revival and continue to check until 80% confluent. Media change can be given if needed.
5. Once confluent passage into an appropriate flask at a density of 2x104 cells/cm2. Seeding density is given as a guide only and should be scaled to align with individual lab schedules. Cultures should be monitored daily.

Subculture guidelines
  • All seeding densities should be based on cell counts gained by established methods.
  • A guide seeding density of 2x104 cells/cm2 is recommended.
  • Cells should be passaged when they have achieved 80-90% confluence.
Culture medium
DMEM (High Glucose) + 10% FBS
Cryopreservation medium
Cell Freezing Medium-DMSO Serum free media, contains 8.7% DMSO in MEM supplemented with methyl cellulose.

Storage

Shipped at conditions
Dry Ice
Appropriate short-term storage conditions
-196°C
Appropriate long-term storage conditions
-196°C

Notes

Recommended control: Human wild-type HEK293T cell line (ab255449). Please note a wild-type cell line is not automatically included with a knockout cell line order, if required please add recommended wild-type cell line at no additional cost using the code WILDTYPE-TMTK1.

We will provide viable cells that proliferate on revival.

This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our limited use license and patent pages.

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.
Activity summary

NADH:ubiquinone oxidoreductase core subunit S3 (NDUFS3) is an important component of the mitochondrial respiratory chain complex I also known as NADH:ubiquinone oxidoreductase. With an approximate mass of 25 kDa NDUFS3 plays an integral role in the assembly and function of complex I. This protein is mostly expressed in the mitochondria across various tissues. It is better known as a core subunit important for the catalytic activity of complex I.

Biological function summary

NDUFS3 participates in cellular respiration by facilitating the electron transfer from NADH to ubiquinone. It is part of the complex I assembly that comprises 45 different subunits. This large assembly is the first enzyme of the mitochondrial electron transport chain and it ensures efficient energy production in the form of ATP. In its role NDUFS3 collaborates closely with other core subunits like NDUFS1 and NDUFS2 to maintain the proper function of cellular metabolism.

Pathways

NDUFS3 is essential in the oxidative phosphorylation pathway which plays an important part in ATP generation. By interacting with other complex I subunits NDUFS3 enables electron flow that drives ATP synthase activity. Additionally it is connected to the apoptosis pathway. Its dysfunction may result in disrupted energy metabolism which can trigger cell death. NDUFS3 also interacts with proteins like NDUFV1 and NDUFV2 highlighting its centrality in energy and signal transduction processes.

Associated diseases and disorders

NDUFS3 links to mitochondrial disorders and neurodegenerative diseases such as Leigh syndrome. Mutations in NDUFS3 can impair mitochondrial function leading to reduced ATP production and accumulation of defective mitochondria. These alterations contribute to the progressive deterioration seen in these disorders. In the context of neurodegenerative diseases NDUFS3 dysfunction may associate with proteins like cytochrome c emphasizing its role in mitochondria-dependent apoptotic pathways and neuronal health.

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