Abcam, ab258654, Human SDHD knockout HEK-293T cell lysate

Size: 1Kit
SDHD KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, Homozygous: 2 bp insertion in exon 1.
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 2 bp insertion in exon 1.

Product details:
Knockout cell lysate achieved by CRISPR/Cas9.
REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.
Lysate preparation:
Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10).
This means that the protein of interest is denatured.
If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions:
Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages

Properties and Storage Information:
Gene name-SDHD, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Zygosity-Homozygous, Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
The SDHD protein also known as succinate dehydrogenase complex subunit D serves a function in cellular respiration. This protein is a part of the succinate dehydrogenase (SDH) complex found in the inner mitochondrial membrane. This complex is known as complex II in the electron transport chain. The subunit D with a mass of about 15 kDa anchors the larger SDH complex to the membrane and is essential for its structural stability. SDHD is widely expressed in tissues with high energy demands such as the heart liver and muscles.
Biological function summary
The SDH complex has an essential role in both the Krebs cycle and the mitochondrial electron transport chain. SDHD as part of this complex assists in the oxidation of succinate to fumarate an important step in the Krebs cycle. The electrons generated from succinate oxidation are transferred through the SDH complex to ubiquinone contributing to ATP production. The complex facilitates the coupling of the Krebs cycle to the electron transport chain highlighting SDHD’s importance in efficient energy metabolism.
Pathways
SDHD integrates into the Krebs cycle and the electron transport chain linking these vital energy-yielding reactions. In the Krebs cycle it assists in converting succinate to fumarate contributing important intermediates and electron donors for oxidative phosphorylation. It interacts with other components of complex II such as SDHA SDHB and SDHC to facilitate its enzymatic functions. Furthermore its role in electron transport involves ubiquinone which carries electrons to complex III continuing the chain of reactions needed for energy production.
SDHD mutations have been linked with paragangliomas and pheochromocytomas both of which are neuroendocrine tumors. These conditions are associated with disrupted cellular energy metabolism caused by impaired function of the SDH complex. In these tumors mutations in SDHD can lead to a pseudohypoxic state promoting cell proliferation. The protein's dysfunction connects pathophysiologically to related SDHB SDHC and SDHA subunits with mutations in these subunits also contributing to the manifestation of such tumors.