WH0168374M1
Monoclonal Anti-ZNF92 antibody produced in mouse
clone 1F2, purified immunoglobulin, buffered aqueous solution
别名:
Anti-HPF12, Anti-TF12, Anti-zinc finger protein 92 (HTF12)
产品名称
Monoclonal Anti-ZNF92 antibody produced in mouse, clone 1F2, purified immunoglobulin, buffered aqueous solution
biological source
mouse
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
1F2, monoclonal
form
buffered aqueous solution
species reactivity
human
technique(s)
indirect ELISA: suitable
western blot: 1-5 μg/mL
isotype
IgG1κ
GenBank accession no.
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Quality Level
Gene Information
human ... ZNF92(168374)
General description
Zinc finger protein 92 (ZNF92) is a transcription factor and the gene encoding it is located on human chromosome 7.
Immunogen
ZNF92 (NP_689839, 490 a.a. ~ 586 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.
Sequence
FNQSSIFTKHKIIHTEGKSYKCEKCGNAFNQSSNLTARKIIYTGEKPYKYEECDKAFNKFSTLITHQIIYTGEKPCKHECGRAFNKSSNYTKEKLQT
Sequence
FNQSSIFTKHKIIHTEGKSYKCEKCGNAFNQSSNLTARKIIYTGEKPYKYEECDKAFNKFSTLITHQIIYTGEKPCKHECGRAFNKSSNYTKEKLQT
Physical form
Solution in phosphate buffered saline, pH 7.4
Legal Information
GenBank is a registered trademark of United States Department of Health and Human Services
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存储类别
10 - Combustible liquids
wgk
nwg
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
法规信息
常规特殊物品
此项目有
Mohana Ray et al.
BMC genomics, 14, 505-505 (2013-07-28)
Solid tumors present a panoply of genomic alterations, from single base changes to the gain or loss of entire chromosomes. Although aberrations at the two extremes of this spectrum are readily defined, comprehensive discernment of the complex and disperse mutational
M Katharine Rudd et al.
Human molecular genetics, 18(16), 2957-2962 (2009-05-16)
Copy number studies have led to an explosion in the discovery of new segmental duplication-mediated deletions and duplications. We have analyzed copy number changes in 2419 patients referred for clinical array comparative genomic hybridization studies. Twenty-three percent of the abnormal
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