MABD51
抗-Brn-2 （POU3F2）抗体，克隆8C4.2
clone 8C4.2, from mouse
别名:
POU domain, class 3, transcription factor 2, Brain-specific homeobox/POU domain protein 2, Brain-2, Brn-2, Nervous system-specific octamer-binding transcription factor N-Oct-3, Octamer-binding protein 7, Oct-7, Octamer-binding transcription factor 7, OTF
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关于此项目
UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Conjugate:
unconjugated
Clone:
8C4.2, monoclonal
Application:
IHC, WB
Citations:
6
biological source
mouse
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
8C4.2, monoclonal
species reactivity
rat, human
technique(s)
immunohistochemistry: suitable (paraffin), western blot: suitable
isotype
IgG1κ
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Quality Level
Gene Information
human ... POU3F2(5454)
General description
Brn-2 （POU结构域，第3类，转录因子2; Oct-7; N-Oct-3; 或POU3F2）是POU 结构域转录因子大家族的成员。 高度同源的POU结构域包含N末端的一个POU特定结构域，C末端的一个POU同源结构域，以及一个互联连接子区。POU 结构域连接 DNA 序列 5’-ATGCAAAT-3’。Brn-2 在发育中的CNS中高度表达，并可能在神经形成，特别是下丘脑的发育中起一定作用。过去的研究也表明 Brn-2 可以整合 BRAF/MAP 激酶和Wnt/β-联蛋途径下游的信号，Brn-2 可能涉及黑色素瘤的转化和增殖。
观测值〜54 kDa。
计算分子量为47 kDa，Brn-2（POU3F2）在一些细胞裂解液中观测值为~50-55 kDa（Wolfe, A., et al., (2002).Molecular Endocrinology.16(3):435-449)。
计算分子量为47 kDa，Brn-2（POU3F2）在一些细胞裂解液中观测值为~50-55 kDa（Wolfe, A., et al., (2002).Molecular Endocrinology.16(3):435-449)。
Immunogen
GST标记的重组蛋白，对应于人Brn-2 (POU3F2)。
Application
免疫组化分析：代表性批次的1：50稀释液可在正常大鼠脑组织、浦肯野细胞、篮细胞、大鼠小脑组织的神经胶质细胞、大鼠小脑组织的神经元、大鼠额叶皮层的神经元和神经胶质细胞以及人脑桥组织的神经元中检测Brn-2。
抗-Brn-2（POU3F2）抗体（克隆8C4.2）可检测Brn-2 （POU3F2）水平，&已发布&经验证可用于蛋白质印迹、IHC(P)。
Physical form
形式：纯化
Analysis Note
对照
SK-N-MC细胞裂解液
SK-N-MC细胞裂解液
通过蛋白质印迹法在 SK-N-MC 细胞裂解液中进行了评估。
蛋白质印迹分析：该抗体的1：2,000稀释液在10 µg SK-N-MC细胞裂解液中检测到Brn-2 (POU3F2)。
蛋白质印迹分析：该抗体的1：2,000稀释液在10 µg SK-N-MC细胞裂解液中检测到Brn-2 (POU3F2)。
Other Notes
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存储类别
12 - Non Combustible Liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Meitetsu Masawa et al.
The American journal of pathology, 192(6), 847-861 (2022-04-04)
Although recent reports have revealed the importance of the inactivation of both RB1 and TP53 in the transformation from lung adenocarcinoma into neuroendocrine carcinoma (NEC), the requirements for complete transformation into NEC have not been elucidated. To investigate alterations in
Zhongyuan Bao et al.
Oxidative medicine and cellular longevity, 2021, 6338722-6338722 (2021-12-03)
Traumatic brain injury (TBI) causes a high rate of mortality and disability, and its treatment is still limited. Loss of neurons in damaged area is hardly rescued by relative molecular therapies. Based on its disease characteristics, we transplanted human embryonic
Yilin Feng et al.
STAR protocols, 4(3), 102346-102346 (2023-07-08)
In glioma modeling, existing organoid protocols lack the ability to replicate glioma cell invasion and interaction with normal brain tissue. Here, we present a protocol for generating in vitro brain disease models using human-induced pluripotent- or embryonic-stem-cell-derived cerebral organoids (COs). We
Waseem K Raja et al.
PloS one, 17(12), e0277532-e0277532 (2022-12-02)
There are currently no preventive or disease-modifying therapies for Parkinson's Disease (PD). Failures in clinical trials necessitate a re-evaluation of existing pre-clinical models in order to adopt systems that better recapitulate underlying disease mechanisms and better predict clinical outcomes. In
Aaron Gordon et al.
Nature neuroscience, 24(3), 331-342 (2021-02-24)
Human stem-cell-derived models provide the promise of accelerating our understanding of brain disorders, but not knowing whether they possess the ability to mature beyond mid- to late-fetal stages potentially limits their utility. We leveraged a directed differentiation protocol to comprehensively
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