Abcam, ab258923, Human INF2 knockout HeLa cell lysate

Size: 1Kit
INF2 KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon2 and 29 bp deletion in exon2 and Insertion of the selection cassette 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, 1 bp insertion in exon2 and 29 bp deletion in exon2 and Insertion of the selection cassette 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, 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-INF2, 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.
The INF2 protein officially named Inverted Formin 2 is involved in actin dynamics. It has a mass of approximately 139 kDa. INF2 exists throughout many tissues in the body with high expression in the kidney brain and heart. This protein structurally influences filamentous actin (F-actin) and globular actin (G-actin) balance facilitating cytoskeleton remodeling and cell shape changes. With these functions INF2 can take on different roles depending on cell type and physiological conditions.
Biological function summary
Inverted Formin 2 acts in multiple cellular processes like cell migration and division. It is a part of the formin family of proteins which are known to regulate actin filament polymerization. INF2 forms complexes with other proteins including mitochondria-associated membranes (MAMs). It connects the endoplasmic reticulum to mitochondria which supports cellular activities like calcium ion transfer and lipid biosynthesis.
Pathways
INF2 interacts with the Rho family GTPases in the regulation of actin cytoskeleton dynamics. It plays important roles in the RhoA pathway assisting the polymerization and depolymerization of actin filaments which impacts cell movement and morphology. INF2 interacts with diaphanous-related formins (DRFs) including mDia1 to support these cellular functions.
Abnormal regulation or mutation of INF2 can lead to serious conditions as shown in focal segmental glomerulosclerosis (FSGS) and Charcot-Marie-Tooth (CMT) disease. Mutations in INF2 causing defective protein interactions can trigger renal pathology by impairing the podocyte cytoskeleton. The connection with nephrin another protein critical for kidney function highlights further implications for FSGS. In neuromuscular disorders like CMT altered dynamics between INF2 and dynamin-related mitochondrial protein (DRP1) affect mitochondrial fission leading to axonal degeneration.