Abcam, ab263380, Human TBC1D7 knockout HeLa cell lysate

Size: 1Kit
TBC1D7 KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 19 bp deletion in exon2 and 2 bp deletion in exon2.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 19 bp deletion in exon2 and 2 bp deletion in exon2.,
Disease:Adenocarcinoma

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 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
patent pages

Properties and Storage Information:
Gene name-TBC1D7, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, 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.
TBC1D7 also known as TRE2-BUB2-CDC16 domain family member 7 is a protein with an approximate mass of 25 kDa. This protein acts as a GAP (GTPase-activating protein) for Rab small GTPases which are involved in intracellular trafficking. The expression of TBC1D7 occurs in various tissues such as the liver skeletal muscle and adipose tissue. With its primary role as a GAP TBC1D7 is significant in regulating Rab GTPases’ cycling between active and inactive states affecting vesicular transport and cellular logistics.
Biological function summary
TBC1D7 functions as a part of the TSC complex consisting of TSC1 (hamartin) TSC2 (tuberin) and TBC1D7. This complex plays a significant role in cellular growth regulation by inactivating the small GTPase Rheb. This action prevents the overactivation of mTORC1 (mechanistic target of rapamycin complex 1) an important controller of cell growth and proliferation. TBC1D7 adds stability to the TSC complex enhancing its ability to regulate mTORC1 activity effectively demonstrating its key role in cellular metabolic regulation.
Pathways
The involvement of the TBC1D7 protein in the mTOR signaling and insulin signaling pathways is well-documented. Within these pathways TBC1D7 operates along with proteins such as Rheb and mTOR itself. By affecting the TSC complex's inhibitory impact on mTORC1 TBC1D7 influences cell growth survival and metabolism. These pathways are essential for energy sensing and management impacting how cells respond to nutrient availability and growth signals.
TBC1D7 has been linked to conditions like Smith-Kingsmore syndrome and tuberous sclerosis complex. In these disorders the TSC complex's ability to regulate mTOR signaling is disrupted. Mutations or dysregulation of TSC1 TSC2 or TBC1D7 itself can lead to unchecked mTOR activation resulting in abnormal cell growth and proliferation. The relationship between TBC1D7 and these conditions highlights its role beyond cellular mechanics influencing pathological states when its function is altered.