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Validated All-in-One™ qPCR Primer for MYO6(NM_004999.3) Search again
Product ID:
HQP011647
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
DFNA22, DFNB37
Gene Description:
myosin VI
Target Gene Accession:
NM_004999.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
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:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene encodes a protein involved intracellular vesicle and organelle transport, especially in the hair cell of the inner ear. Mutations in this gene have been found in patients with non-syndromic autosomal dominant and recessive hearing loss.
Gene References into function
- In families with recessively inherited deafness, DFNB37, our sequence analyses of MYO6 reveal a frameshift mutation (36-37insT), a nonsense mutation (R1166X), and a missense mutation (E216V)
- Results report the effects of the C442Y mutation on the kinetics of the actomyosin ATP hydrolysis mechanism and motor function of myosin VI.
- Inhibiting myosin VI expression in high-grade ovarian carcinoma cells impeded cell spreading and migration in vitro; optical imaging and histopathologic studies revealed that inhibiting myosin VI expression reduces tumor dissemination in nude mice
- myosin VI and Dab2 facilitate CFTR endocytosis by a mechanism that requires actin filaments
- a novel function for p53 in the maintenance of Golgi complex integrity and for myosin VI in the p53-dependent prosurvival pathway.
- Myosin VI modulates RNAPII-dependent transcription of active genes, implicating the possibility of an actin-myosin based mechanism of transcription.
- These results support that myosin VI is critical in maintaining the malignant properties of the majority of human prostate cancers diagnosed today.
- We have identified three binding sites in the Myosin VI carboxy-terminal: a WWY motif for Disabled-2, a RRL motif for glucose-transporter binding protein and optineurin binding and a site that binds specifically to PtdIns(4,5)P2-containing liposomes.
- results suggest that myosin VI-T6BP-NDP52 complexes may play a role in coordinating cytokine signalling and membrane transport pathways with actin filament organisation and cell adhesion
- Results are consistent with vesicle-associated myosin VI existing as a processive dimer, capable of its known trafficking function.
- Myosin VI and LMTK2 are required for the transport of cargo, such as the Transferrin Receptor, from early endosomes to the endocytic recycling compartment.
- inner ear hair cells are sensitive to changes in expression levels of MYO6
- In conclusion, a novel nonsense MYO6 mutation causes post-lingual, slowly progressive autosomal dominant nonsyndromic moderate to severe hearing loss in a Danish family.
- Results show that BREK is critical for the transition of endocytosed membrane vesicles from early endosomes to recycling endosomes and also suggest an involvement of myosin VI in this pathway.
- Golgi apparatus in prostate cancer cells differs from the normal Golgi by elevated levels of two molecules, GOLPH2 and MYO6.