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- 详细信息
- 文献和实验
- 技术资料
- 免疫原:
KLH-conjugated synthetic peptide encompassing a sequence within the center region of human p16-INK4.
- 亚型:
Rabbit Ig
- 形态:
Each vial contains 0.1 mg IgG in 0.1 ml (1 mg/ml) of PBS pH7.4, 25% glycerol, 5 mg/ml BSA with 0.09% sodium azide. Antibody was purified by Protein-A affinity chromatography.
- 保存条件:
Store at -20°C.
- 克隆性:
多克隆抗体
- 标记物:
见下方详细说明
- 适应物种:
H, M, R, D, P, Ck
- 宿主:
Rabbit
- 应用范围:
E, WB, IHC
- 浓度:
见详细说明信息
- 靶点:
p16-INK4
- 抗体英文名:
p16-INK4 Antibody
- 抗体名:
p16-INK4 Antibody
- 规格:
0.1 mg
p16-INK4 Antibody产品详细介绍:
| 产品名称: | p16-INK4 Antibody |
| 说明书: | http://www.abbiotec.com/antibodies/p16-ink4-antibody【参考图片】 |
| 货号: | 250804 |
| 规格: | 0.1 mg |
| 产品描述: | The cyclin-dependent kinase 4 inhibitor A (CDK4I or p16-INK4) acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6 and by subsequently inhibiting their interaction with cyclins D and retinoblastoma protein phosphorylation. Defects in p16-INK4 are involved in tumor formation in a wide range of tissues. These defects cause cutaneous malignant melanoma 2 (CMM2), familial atypical multiple mole melanoma-pancreatic carcinoma syndrome, melanoma-astrocytoma syndrome and Li-Fraumeni syndrome. |
| 克隆类型: | Rabbit Polyclonal Antibody |
| 亚型: | Rabbit Ig |
| 免疫原: | KLH-conjugated synthetic peptide encompassing a sequence within the center region of human p16-INK4. |
| 适用物种: | H, M, R, D, P, Ck |
| 应用范围: | E, WB, IHC |
| 应用说明: | E: 1:500-1:1,000; WB: 1:100-1:500; IHC: 1:100-1:500 |
| 别名: | Cyclin-dependent kinase inhibitor 2A, isoforms 1/2/3; cyclin-dependent kinase inhibitor A; CDK4I; p16-INK4a; p16INK4A; p16-INK4; multiple tumor suppressor 1; MTS-1; CDKN2A; CDKN2; MTS1 |
| 形态: | Each vial contains 0.1 mg IgG in 0.1 ml (1 mg/ml) of PBS pH7.4, 25% glycerol, 5 mg/ml BSA with 0.09% sodium azide. Antibody was purified by Protein-A affinity chromatography. |
| 保存条件: | Store at -20°C. Minimize freeze-thaw cycles. Product is guaranteed one year from the date of shipment. |
| 参考文献: | [1] Chinzei N et al. 2015. Mol Med Rep. 11(3): 1601-8. PMID# 25376471. [2] Jackson L et al. 2011. Cellular Immunology. 272(2): 200-213. PMID# 22078270. |
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文献和实验p16INK4A and Familial Melanoma
. This phase is controlled by several protein complexes including those consisting of cyclin-dependent kinases (CDK4 and CDK6) and cyclin D. These complexes are inhibited by the INK4 family of proteins—p16INK4A , p15INK4B , p18INK4C , and p19INK4D . Genetic
Analysis of p16INK4a and Integrated HPV Genomes as Progression Markers
that never develop a lesion. Only a small percentage of low-grade dysplasias finally grow out to invasive cancer. Several biomarkers can be used to identify lesions at risk for malignant progression. Overexpression of p16INK4a is induced by the viral oncoprotein E7
Sensitive Detection of Hypermethylated p16INK4a Alleles in Exfoliative Tissue Material
Epigenetic DNA modification by aberrant methylation of cytosine residues is thought to be an important mechanism contributing to tumorigenesis. Methylation of cytosines normally occurs at distinct sites of the genome containing stretches
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