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生物源
mouse
品質等級
共軛
unconjugated
抗體表格
purified immunoglobulin
抗體產品種類
primary antibodies
無性繁殖
polyclonal
形狀
buffered aqueous solution
分子量
antigen ~77.2 kDa
物種活性
human
技術
indirect immunofluorescence: suitable
western blot: 1 μg/mL
NCBI登錄號
UniProt登錄號
運輸包裝
dry ice
儲存溫度
−20°C
目標翻譯後修改
unmodified
基因資訊
human ... CUX1(1523)
一般說明
Cut homeobox 1 (CUX1) is a transcription factor that contains three major domains, which include four DNA binding domains, three CUT domains or repeats (C1, C2, and C3), and a Cut homeodomain. It is expressed in multiple isoforms.
免疫原
CUX1 (AAH25422.1, 1 a.a. ~ 676 a.a) full-length human protein.
Sequence
MAANVGSMFQYWKRFDLQQLQRELDATATVLANRQDESEQSRKRLIEQSREFKKNTPEDLRKQVAPLLKSFQGEIDALSKRSKEAEAAFLNVYKRLIDVPDPVPALDLGQQLQLKVQRLHDIETENQKLRETLEEYNKEFAEVKNQEVTIKALKEKIREYEQTLKNQAETIALEKEQKLQNDFAEKERKLQETQMSTTSKLEEAEHKVQSLQTALEKTRTELFDLKTKYDEETTAKADEIEMIMTDLERANQRAEVAQREAETLREQLSSANHSLQLASQIQKAPDVAIEVLTRSSLEVELAAKEREIAQLVEDVQRLQASLTKLRENSASQISQLEQQLSAKNSTLKQLEEKLKGQADYEEVKKELNILKSMEFAPSEGAGTQDAAKPLEVLLLEKNRSLQSESAALRISNSDLSGRCAELQVRITEAVATATEQRELIARLEQDLSIIQSIQRPDAEGAAEHRLEKIPEPIKEATALFYGPAAPASGALPEGQVDSLLSIISSQRERFRARNQELEAENRLAQHTLQALQSELDSLRADNVKLFEKIKFLQSYPGRGSGSDDTELRYSSQYEERLDPFSSFSKRERQRKYLSLSPWDKATLSMGRLVLSNKMARTIGFFYTLFLHCLVFLVLYKLAWSESMERDCATFCAKKFADHLHKFHENDNGAAAGDLWQ
Sequence
MAANVGSMFQYWKRFDLQQLQRELDATATVLANRQDESEQSRKRLIEQSREFKKNTPEDLRKQVAPLLKSFQGEIDALSKRSKEAEAAFLNVYKRLIDVPDPVPALDLGQQLQLKVQRLHDIETENQKLRETLEEYNKEFAEVKNQEVTIKALKEKIREYEQTLKNQAETIALEKEQKLQNDFAEKERKLQETQMSTTSKLEEAEHKVQSLQTALEKTRTELFDLKTKYDEETTAKADEIEMIMTDLERANQRAEVAQREAETLREQLSSANHSLQLASQIQKAPDVAIEVLTRSSLEVELAAKEREIAQLVEDVQRLQASLTKLRENSASQISQLEQQLSAKNSTLKQLEEKLKGQADYEEVKKELNILKSMEFAPSEGAGTQDAAKPLEVLLLEKNRSLQSESAALRISNSDLSGRCAELQVRITEAVATATEQRELIARLEQDLSIIQSIQRPDAEGAAEHRLEKIPEPIKEATALFYGPAAPASGALPEGQVDSLLSIISSQRERFRARNQELEAENRLAQHTLQALQSELDSLRADNVKLFEKIKFLQSYPGRGSGSDDTELRYSSQYEERLDPFSSFSKRERQRKYLSLSPWDKATLSMGRLVLSNKMARTIGFFYTLFLHCLVFLVLYKLAWSESMERDCATFCAKKFADHLHKFHENDNGAAAGDLWQ
生化／生理作用
Cut homeobox 1 (CUX1) binds to DNA and is involved in DNA repair. It stimulates the 8-oxoguanine-DNA glycosylase 1 (OGG1), a prime enzyme that acts on oxidative purine lesions and may have an indirect influence on radioresistance. Haploinsufficiency of CUX1 may have an impact on developmental delay (DD) and mild intellectual disability(ID). The multiple isoforms of CUX1 may have implications on various physiological pathologies like polycystic kidney disease and tumor development. In cortical neurons, CUX1 may play a key role in regulating spine development, dendritic branching, and synapse formation. CUX1 is a tumor suppressor gene and its deletion is implicated in high-risk acute myeloid leukemia.
外觀
Solution in phosphate buffered saline, pH 7.4
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
10 - Combustible liquids
水污染物質分類（WGK）
WGK 1
閃點（°F）
Not applicable
閃點（°C）
Not applicable
Megan E McNerney et al.
Blood, 121(6), 975-983 (2012-12-06)
Loss of chromosome 7 and del(7q) [-7/del(7q)] are recurring cytogenetic abnormalities in hematologic malignancies, including acute myeloid leukemia and therapy-related myeloid neoplasms, and associated with an adverse prognosis. Despite intensive effort by many laboratories, the putative myeloid tumor suppressor(s) on
Zubaidah M Ramdzan et al.
Oncotarget, 8(12), 19021-19038 (2017-02-02)
Ionizing radiation generates a broad spectrum of oxidative DNA lesions, including oxidized base products, abasic sites, single-strand breaks and double-strand breaks. The CUX1 protein was recently shown to function as an auxiliary factor that stimulates enzymatic activities of OGG1 through
Konrad Platzer et al.
Annals of neurology, 84(2), 200-207 (2018-07-18)
Developmental delay (DD) with favorable intellectual outcome and mild intellectual disability (ID) are mostly considered to be of complex genetic and environmental origin, but, in fact, often remain unclear. We aimed at proving our assumption that also mild cases of
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