Abcam, ab257648, Human RUNX1 (AML1) knockout HeLa cell lysate

Size: 1Kit
MECOM KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 86 bp insertion in exon4.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 86 bp insertion in exon4.,
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-MECOM, 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.
RUNX1 also known as AML1 is a transcription factor with a molecular weight of approximately 48 kDa. It belongs to the Runt-related transcription factor family and plays a critical role in hematopoiesis. RUNX1 is expressed in hematopoietic stem cells and various other tissues where it regulates the expression of genes involved in the differentiation and proliferation of blood cells. It exerts its function by binding to specific DNA sequences thereby controlling the transcriptional activity necessary for normal hematopoietic development.
Biological function summary
RUNX1 is essential in the formation of blood cells and is part of the core-binding factor (CBF) complex. This complex is a heterodimer comprising RUNX1 and the CBFβ subunit. The interaction between RUNX1 and CBFβ stabilizes the DNA binding capability of RUNX1 facilitating the activation of target gene transcription. The proper functioning of RUNX1 is necessary for the maintenance of normal lineage specification of hematopoietic progenitors affecting both myeloid and lymphoid cell lineages.
Pathways
RUNX1 plays a significant role in the Wnt signaling pathway and the TGF-beta signaling pathway. RUNX1 interacts with several proteins in these pathways including SMAD proteins and β-catenin which are important for transmitting extracellular signals that regulate cell growth and differentiation. RUNX1’s role in these pathways highlights its importance not only in hematopoiesis but also in preventing abnormal cell proliferation.
RUNX1 mutations are strongly associated with acute myeloid leukemia (AML) and familial platelet disorder. In AML RUNX1 mutations disrupt normal hematopoiesis leading to the uncontrolled proliferation of immature blood cells. RUNX1-related proteins such as the GM-CSF receptor can contribute to disease progression by altering cytokine signaling. RUNX1's involvement in familial platelet disorder reflects its importance in maintaining normal blood cell counts and function as loss of RUNX1 function leads to predisposition to leukemia.