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Validated All-in-One™ qPCR Primer for PRDM16(NM_022114.3) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
The reciprocal translocation t(1;3)(p36;q21) occurs in a subset of myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). This gene is located near the 1p36.3 breakpoint and has been shown to be specifically expressed in the t(1:3)(p36,q21)-positive MDS/AML. The protein encoded by this gene is a zinc finger transcription factor and contains an N-terminal PR domain. The translocation results in the overexpression of a truncated version of this protein that lacks the PR domain, which may play an important role in the pathogenesis of MDS and AML. Alternatively spliced transcript variants encoding distinct isoforms have been reported. [provided by RefSeq].
Gene References into function
- Breakpoints occurring in the first intron and in the 5' region of the MEL1 gene associated with the t(1;3)(p36;q21) translocation have been found in three myelodysplastic syndrome/acute myelogenous leukemia patients.
- structure, expression pattern, and function of MEL1 in leukemia cells; overexpression of the zinc finger protein lacking the PR domain (EVI1 and MEL1S)is likely one of the causative factors in the pathogenesis of myeloid leukemia.
- Aberrant gene expression associated with DNA hypomethylation is implicated in leukemogenesis of adult T-cell leukemia.
- Correction opf X-linked chronic granulomatous disease by gene therapy was augmented by insertional activation of PRDM16.
- A 3' RACE experiments followed by sequence-specific RT-PCR resulted in the identification of the PRDM16 gene as a novel fusion partner of the RUNX1 gene in a patient with rare t(1;21)(p36;q22).
- RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance
- array CGH performed on CD34(+) cells revealed cryptic partial deletions of PRDM16.
