Abcam, ab259189, Human TMEM165 knockout HEK-293T cell lysate

Size: 1Kit
TMEM165 KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 2 bp insertion in exon1.
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 2 bp insertion in exon1.

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-TMEM165, 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.
TMEM165 also known as Transmembrane Protein 165 or TMPTD is a transmembrane protein with an approximate molecular mass of 41 kDa. This protein predominantly localizes to the Golgi apparatus where it plays a mechanical function as a cation transporter. Expression of TMEM165 is wide with the protein being found in various tissues but with higher representation in certain organs including the heart and liver. Its structure comprises multiple transmembrane domains contributing to its role in maintaining ion homeostasis within the organelles.
Biological function summary
TMEM165 maintains the balance of ions within the Golgi apparatus influencing glycosylation processes. It is part of a complex that includes ion channels and other transporters essential for the proper modification of proteins through glycosylation. Alterations in TMEM165 function could affect the fidelity of these protein modifications impacting cell signaling and function. These roles emphasize TMEM165's importance in cellular activities that rely on precisely glycosylated proteins.
Pathways
TMEM165 plays significant roles in both glycosylation and electrolyte balance within the Golgi apparatus. It participates in pathways related to calcium and manganese ion homeostasis important for Golgi functions and protein processing. The protein interacts with other ion transporters and channels such as ATP2C1 to facilitate these processes. These interactions support proper folding and processing of glycoproteins which is integral to maintaining cellular and tissue homeostasis.
The malfunction of TMEM165 links to complex syndromes such as Congenital Disorder of Glycosylation (CDG) where improper protein glycosylation occurs. Mutations in the TMEM165 gene result in defective glycosylation leading to various clinical manifestations. Another disorder related to TMEM165 is characterized by bone development issues possibly connected to its role in manganese transport. Researchers have also observed interactions with TMEM51 regarding skeletal abnormalities indicating a shared pathway alteration contributing to disease development.