PLA0039
Goat anti-MCM4 Antibody, Affinity Purified
Powered by Bethyl Laboratories, Inc.
别名:
CDC21, CDC21 homolog, CDC54, MCM4 minichromosome maintenance deficient 4 (S. cerevisiae), MGC33310, NKCD, NKGCD, P1-Cdc21, hCdc21, homolog of S. pombe cell devision cycle 21, minichromosome maintenance deficient 4
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About This Item
生物源
goat
品質等級
抗體表格
affinity purified immunoglobulin
抗體產品種類
primary antibodies
等級
Powered by Bethyl Laboratories, Inc.
物種活性
mouse, human
技術
immunohistochemistry: 1:500-1:2,000
western blot: 1:2,000-1:10,000
登錄號
NP_005905.2
UniProt登錄號
運輸包裝
wet ice
儲存溫度
2-8°C
基因資訊
goat ... MCM4(4173)
免疫原
The epitope recognized by PLA0039 maps to a region between residues 325 and 375 of human Minichromosome Maintenance 4 using the numbering given in entry NP_005905.2 (GeneID 4173).
外觀
Tris-citrate/phosphate buffer, pH 7 to 8 containing 0.09% sodium azide
其他說明
The MCM (Mini-Chromosome Maintenance) complex is a key component of the pre-replication complex involved in replication licensing which restricts DNA replication to only once per cell cycle. The MCM complex is a heterohexamer of MCM2, MCM3, MCM4, MCM5, MCM6, and MCM7. MCM4 is part of the core MCM complex that includes MCM4, MCM6, and MCM7. The core complex possesses DNA helicase activity. MCM4 is phosphorylated by CDC2 kinase resulting in a reduction of helicase activity and chromatin binding.
免責聲明
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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儲存類別代碼
12 - Non Combustible Liquids
水污染物質分類(WGK)
nwg
閃點(°F)
Not applicable
閃點(°C)
Not applicable
Nucleic acids research, 42(9), 5605-5615 (2014-03-05)
Accumulating evidence suggests that dormant DNA replication origins play an important role in the recovery of stalled forks. However, their functional interactions with other fork recovery mechanisms have not been tested. We previously reported intrinsic activation of the Fanconi anemia
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