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. Author manuscript; available in PMC: 2010 Dec 1.
Published in final edited form as: Exp Hematol. 2009 Oct 6;37(12):1411–1422. doi: 10.1016/j.exphem.2009.09.009

Figure 1. Detection of JAK2V617F mutation in primary erythroid precursors.

Figure 1

Total RNA isolated from primary erythroblasts of healthy controls and PV patients was reverse transcribed followed by PCR amplification for JAK2 yielding a 566 bp product. (A) Detection of JAK2V617F by restriction enzyme BsaXI digestion. The wild-type allele is digested into 354, 212, and 182 bp fragments whereas the mutant allele, detected only in PV patients, remains undigested. The allele-burden of JAK2V617F in PV patients was quantified by densitometry and expressed as percentage. (B) Sequence traces illustrating wild-type sequence (a healthy control) and confirmation of mixed G>T sequences in a representative patient with PV. The presence of the mutant JAK2V617F allele was confirmed by direct sequencing in all patient samples.