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Merck
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Key Documents

PLA0039

Sigma-Aldrich

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

分類程式碼代碼:
12352203
NACRES:
NA.41

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


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Spencer W Luebben et al.
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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