Principle 

The JAK2 gene encodes a protein essential for blood cell growth and differentiation. The common JAK2 V617F mutation leads to overactive JAK2 kinase, causing excessive blood cell production and contributing to myeloproliferative neoplasms (MPNs) such as polycythemia vera and essential thrombocythemia. This gain-of-function mutation disrupts regulatory control, resulting in constant activation of signaling pathways like JAK/STAT, PI3K/AKT, and MAPK, which promote unchecked myeloid cell proliferation.

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JAK2 V617F drives cytokine-independent cell growth, especially when co-expressed with homodimeric receptors like EPOR, and induces persistent STAT5 activation, increased DNA damage, genomic instability, and an inflammatory environment that fuels disease progression. It also impacts gene expression via nuclear activities affecting chromatin. Understanding this mutation’s complex biology is critical for studying MPNs and developing targeted therapies.

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Our cell lines were generated using a human JAK2 overexpression vector co-expressing hygromycin resistance and GFP, ensuring easy selection and visualization. SL-0202 was co-transfected with an additional EPOR overexpression vector co-expressing G418 resistance. Single clones were established through rigorous hygromycin selection and GFP sorting, and thoroughly validated by PCR sequencing and western blotting with JAK-specific antibodies for authenticity and reproducibility.