The primer mix has been verified to generate satisfactory qPCR data on Roche Applied-science LightCycler® 480 Ⅱ.
Storage & Shipping
Lyophilized qPCR primer mix is shipped at ambiente temperatura
The lyophilized product is stable for one year from date of receipt when stored at -20℃.
The suspended product is stable for six months from date of receipt when stored at -20℃.
***Sino biological qEASY qPCR primer pairs are used for SYBR Green-based real-time RT-PCR, The primers are designed by using SBI's proprietary primer design algorithm. Our primer collection covers the entire human genomes. It can be widely applied in the quantitative analysis of gene expression.***
Features and Advantages
Unique Primer Design
To avoid genomic DNA amplification, at least one primer is designed crosses the junction of exons according to the conserved region of a specific gene with all variants.
Strict Validation Process
Confirmed in positive organizations; screened the primer with high specificity and high sensitivity.
Uniform PCR conditions, Saving time and cost
~100% amplification curve, ensuring the accuracy of the RNA quantitative
Human BMP4 qPCR Primer Pair: Synonyms
BMP2B qPCR Primer Pairs, Human; BMP2B1 qPCR Primer Pairs, Human; MCOPS6 qPCR Primer Pairs, Human; OFC11 qPCR Primer Pairs, Human; ZYME qPCR Primer Pairs, Human
BMP4 Background Information
BMP4 (bone morphogenetic protein-4)-directed differentiation of human embryonic stem cells (ESCd). Autophagy is a conserved catabolic process with complicated roles in tumor development. Bone morphogenetic protein 4 (BMP4), a member of the transforming growth factor (TGF-β) family of regulatory proteins, plays a crucial role in human malignancies. BMP4 treatment promoted HCC cells proliferation and induced autophagy. Mechanistic study revealed that the induction of autophagy by BMP4 was mediated through activating the JNK1/Bcl2 pathway. And the JNK1 inhibitor and knockdown of JNK1 could attenuate autophagy induced by BMP4 and eliminated BMP4-promoted HCC cells growth. BMP4 promoted HCC proliferation by autophagy activation through JNK1/Bcl-2 signaling.
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