Abcam, ab257482, Human INA (alpha Internexin) knockout HeLa cell lysate

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INA KO cell lysate available now. KO validated by Western blot. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 179 bp deletion in exon1 and 1 bp insertion in exon1.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 179 bp deletion in exon1 and 1 bp insertion in exon1.,
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-INA, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, 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.
Alpha Internexin also known as alpha-Int or INA is a neuronal intermediate filament protein with a molecular mass of approximately 66 kDa. It plays a significant role in the formation of the neuronal cytoskeleton providing structural support to axons. Alpha Internexin is expressed mainly in the central nervous system and is found in neurons throughout the brain and spinal cord. Despite sharing functions with other intermediate filament proteins like NF-L alpha Internexin is unique in its distribution and timing of expression during neural development.
Biological function summary
Alpha Internexin contributes to the composition of the neurofilament complex which includes proteins like NF-M NF-L and NF-H. This complex stabilizes neuronal architecture and ensures the integrity of the axonal structure. Presence of alpha Internexin is important for maintaining the dynamic processes of axonal transport and neuron stability. It acts as a scaffolding that supports cellular transport mechanisms important for neuron function and survival especially in developing neurons where it leads the polymerization of other neurofilaments.
Pathways
Alpha Internexin interacts within the neurofilament network a major scaffolding component of neurons. It associates with microtubule-associated proteins influencing axonal growth and stabilization pathways. Moreover it plays a part in the MAPK (mitogen-activated protein kinases) signaling pathways which regulate diverse cellular activities such as proliferation and differentiation. Its interactions with related proteins such as plectin and dynein highlight its role in crosslinking cytoskeletal components and facilitating intracellular transport.
Alpha Internexin has been implicated in neurodegenerative conditions such as Amyotrophic Lateral Sclerosis (ALS) and Alzheimer's disease. Misregulation or mutation in alpha Internexin can contribute to the pathological hallmarks of these diseases including protein aggregation and neuronal death. In ALS the presence of alpha Internexin inclusions correlates with disease pathology alongside other neurofilament proteins like NF-L. In Alzheimer's disease abnormal phosphorylation and aggregation of alpha Internexin are associated with neurofibrillary tangles which are indicative of neuronal injury and loss.