产品名称
MISSION® esiRNA, targeting human E2F6
description
Powered by Eupheria Biotech
product line
MISSION®
form
lyophilized powder
esiRNA cDNA target sequence
GCAACTGATGGCATTTGAGAATTTATGTATCACTGAGTTTTTTGGGAATATCTTCGTGGAGAATTACGCATCAAATTTGATTCTCAGAGCAATAAATTATCCATGAAGTGCTCTCGTTCTCAGTAGCGGCATCATGGCCAGTAGTGTCTTTGAGGAGTTCACCACTTAGATTACTGAGTAATTGTGGTTTCCACATTTGAAAACAACTCCTTTTATAATTATTCACTGCTTTTTGTCAGTGAAATAGACATCTTGCCTCCTGAAGTAGCTTCATCACAGAGTGTCATGAAGACAGACAGTCAGGCTGAAATGGACAGTTCTTTGTGGACTCTACCCTTCCCTTCAAGGAGTATGTCATATATCACAAAAGAAATTGCCTTACACTGGTTCATGTTTGCAGTT
Ensembl | human accession no.
NCBI accession no.
shipped in
ambient
storage temp.
−20°C
Quality Level
Gene Information
human ... E2F6(1876), E2F6(1876)
General description
MISSION esiRNA are endoribonuclease prepared siRNA. They are a heterogeneous mixture of siRNA that all target the same mRNA sequence. These multiple silencing triggers lead to highly-specific and effective gene silencing.
For additional details as well as to view all available esiRNA options, please visit SigmaAldrich.com/esiRNA.
For additional details as well as to view all available esiRNA options, please visit SigmaAldrich.com/esiRNA.
Legal Information
MISSION is a registered trademark of Merck KGaA, Darmstadt, Germany
存储类别
10 - Combustible liquids
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
BAP1 immunohistochemistry and p16 FISH to separate benign from malignant mesothelial proliferations.
Brandon S Sheffield et al.
The American journal of surgical pathology, 39(7), 977-982 (2015-01-31)
A variety of immunohistochemical (IHC) stains have been proposed to mark either benign or malignant mesothelial proliferations. Loss of the p16 tumor suppressor (CDKN2A), through homozygous deletions of 9p21, is a good marker of mesotheliomas but lacks sensitivity. Recent reports
Betheney R Pennycook et al.
Nature communications, 11(1), 3503-3503 (2020-07-16)
DNA replication timing is tightly regulated during S-phase. S-phase length is determined by DNA synthesis rate, which depends on the number of active replication forks and their velocity. Here, we show that E2F-dependent transcription, through E2F6, determines the replication capacity
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