Ki67 qPCR Primer Pairs, Human

Cat: HP101766
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Ki67 qPCR Primer Pairs, Human General Information
Target Details
Species:
Human
Product Details
Oligo-Type:
qPCR Primers
Component:
1 vial of lyophilized qPCR primer mix (1 nmol each primer, sufficient for 200 numbers of 25 μl reactions).
QPCR Primer Description:
Verified forward and reverse primers for analyzing the quantitative expression of gene.
Application & Quality
Application:
SYBR® Green-based quantitative real-time PCR (qPCR).
Quality Control:
The primer mix has been verified to generate satisfactory qPCR data on Roche Applied-science LightCycler® 480 Ⅱ.
Storage & Shipping
Shipping:
Lyophilized qPCR primer mix is shipped at ambiente temperatura
Storage:
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
Ki67 qPCR Primer Pairs, Human Alternative Names
KIA qPCR Primer Pairs, Human;MIB- qPCR Primer Pairs, Human;MIB-1 qPCR Primer Pairs, Human;PPP1R105 qPCR Primer Pairs, Human
Ki67 Background Information

MKI67 contains 1 FHA domain and plays a key role in cell proliferation. During interphase, the MKI67 antigen can be exclusively detected within the cell nucleus, whereas in mitosis most of the protein is relocated to the surface of the chromosomes. MKI67 protein is present during all active phases of the cell cycle (G1, S, G2, and mitosis), but is absent from resting cells. MKI67 is an excellent marker to determine the growth fraction of a given cell population. The fraction of MKI67-positive tumor cells is often correlated with the clinical course of cancer. It is also associated with ribosomal RNA transcription. Inactivation of antigen MKI67 leads to inhibition of ribosomal RNA synthesis.

The MKI67 protein is a nuclear and nucleolar protein, which is tightly associated with somatic cell proliferation. Antibodies raised against the human MKI67 protein paved the way for the immunohistological assessment of cell proliferation, particularly useful in numerous studies on the prognostic value of cell growth in clinical samples of human neoplasms. MKI67 protein expression is an absolute requirement for progression through the cell-division cycle. Recently, MKI67 is proved be an independent prognostic factor for disease-free survival (HR 1.05-1.72) in multivariate analyses studies using samples from randomized clinical trials with secondary central analysis of the biomarker. MKI67 was not found to be predictive for long-term follow-up after chemotherapy. Nevertheless, high KI-67 was found to be associated with immediate pathological complete response in the neoadjuvant setting, with an LOE of II-B. MKI67 could be considered as a prognostic biomarker for therapeutic decision.

Full Name
marker of proliferation Ki-67
References
  • Rahmanzadeh R, et al. (2007) Chromophore-assisted light inactivation of pKi-67 leads to inhibition of ribosomal RNA synthesis. Cell Prolif. 40(3):422-30.
  • Bullwinkel J, et al. (2006) Ki-67 protein is associated with ribosomal RNA transcription in quiescent and proliferating cells. J Cell Physiol. 206(3):624-35.
  • Schonk DM, et al. (1989) Assignment of the gene(s) involved in the expression of the proliferation-related Ki-67 antigen to human chromosome 10. Hum Genet. 83(3):297-9.
  • Endl E, et al., 2000, Exp Cell Res. Jun 15;257(2): 231-7.
  • Luporsi E, et al., 2012, Breast Cancer Res Treat. 132(3): 895-915.
  • Scholzen T, et al., 2000, J Cell Physiol. 182(3): 311-22.
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