产品名称
Goat anti-MCM4 Antibody, Affinity Purified, Powered by Bethyl Laboratories, Inc.
biological source
goat
conjugate
unconjugated
antibody form
affinity purified immunoglobulin
antibody product type
primary antibodies
clone
polyclonal
species reactivity
mouse, human
technique(s)
immunohistochemistry: 1:500-1:2,000
western blot: 1:2,000-1:10,000
accession no.
NP_005905.2
UniProt accession no.
shipped in
wet ice
storage temp.
2-8°C
target post-translational modification
unmodified
Quality Level
Gene Information
goat ... MCM4(4173)
Disclaimer
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.
Immunogen
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).
Other Notes
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.
Physical form
Tris-citrate/phosphate buffer, pH 7 to 8 containing 0.09% sodium azide
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存储类别
12 - Non Combustible Liquids
wgk
nwg
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
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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