PLA0178
Rabbit anti-p16INK4a Antibody, Affinity Purified
Powered by Bethyl Laboratories, Inc.
别名:
ARF, CDK4 inhibitor p16-INK4, CDK4I, CDKN2, CMM2, INK4, INK4a, MLM, MTS-1, MTS1, TP16, alternative reading frame, cell cycle negative regulator beta, cyclin-dependent kinase 4 inhibitor A, cyclin-dependent kinase inhibitor 2A (melanoma; p16; inhibits CDK4), multiple tumor suppressor 1, p14, p14ARF, p16, p16-INK4, p16INK4a, p19, p19Arf
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所有图片(1)
About This Item
UNSPSC代码:
12352203
NACRES:
NA.41
推荐产品
生物来源
rabbit
质量水平
抗体形式
affinity purified immunoglobulin
抗体产品类型
primary antibodies
等级
Powered by Bethyl Laboratories, Inc.
种属反应性
human
浓度
0.2 mg/mL
技术
immunohistochemistry: 1:100-1:500
immunoprecipitation (IP): 2-10 μg/mg
western blot: 1:2,000- 1:10,000
登记号
AAA92554.1
运输
wet ice
储存温度
2-8°C
靶向翻译后修饰
unmodified
基因信息
rabbit ... p16INK4a(1029)
一般描述
Cyclin-dependent kinase inhibitor 2A (CDK4I) or p16INK4a belongs to the Ink4 family of CDK inhibitors. The p16INK4agene is mapped to human chromosome 9p21. Structurally, p16INK4a comprises four ankyrin-type repeats (I–IV) .
免疫原
The epitope recognized by PLA0178 maps to a region between residue 106 and 156 of human CDK4 inhibitor p16-INK4a using the numbering given in entry AAA92554.1 (GeneID 1029).
生化/生理作用
Cyclin-dependent kinase inhibitor 2A (CDK4I) or p16INK4a is a negative regulator of cyclin dependant kinase 4 (CDK4) and CDK6 kinase activity and cell cycle progression. The ankyrin repeats (I–IV) are crucial for their interaction with CDK4 and CDK6. P16INK4a regulates the cell cycle by inhibiting cyclin/CDK complex formation and the phosphorylation of the retinoblastoma protein (pRb). P16INK4a is a tumor suppressor and its mutations are associated with malignancies such as melanoma and astrocytoma and are the cause of Li-Fraumeni syndrome.
外形
Tris-buffered Saline containing 0.1% BSA containing 0.09% Sodium Azide
其他说明
p16INK4a is a negative regulator of CDK4 and CDK6 kinase activity and cell cycle progression. P16INK4a regulates the cell cycle by inhibiting cyclin/CDK complex formation and the phosphorylation of the retinoblastoma protein (pRb). P16INK4a is a tumor suppressor associated with malignancies such as melanoma and astrocytoma and is the cause of Li-Fraumeni syndrome.
免责声明
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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储存分类代码
12 - Non Combustible Liquids
WGK
WGK 1
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
常规特殊物品
p16INK4a: a central player in cellular senescence and a promising aging biomarker in elderly cancer patients
Vandenberk B, et al.
2009 IEEE 3rd International Conference on Nano/Molecular Medicine and Engineering, 2(4) (2011)
Sock Hoai Chan et al.
NPJ genomic medicine, 1, 16015-16015 (2016-06-01)
Li-Fraumeni syndrome (LFS) is a rare cancer predisposition syndrome usually associated with TP53 germline alterations. Its genetic basis in TP53 wild-type pedigrees is less understood. Using whole-genome sequencing, we identified a germline hemizygous deletion ablating CDKN2A-CDKN2B in a TP53 wild-type
Caroline Kannengiesser et al.
Human mutation, 30(4), 564-574 (2009-03-05)
Germline mutations of the CDKN2A gene are found in melanoma-prone families and individuals with multiple sporadic melanomas. The encoded protein, p16(INK4A), comprises four ankyrin-type repeats, and the mutations, most of which are missense and occur throughout the entire coding region
C Romagosa et al.
Oncogene, 30(18), 2087-2097 (2011-02-08)
p16(Ink4a) is a protein involved in regulation of the cell cycle. Currently, p16(Ink4a) is considered a tumor suppressor protein because of its physiological role and downregulated expression in a large number of tumors. Intriguingly, overexpression of p16(Ink4a) has also been
David Machover et al.
The Journal of pharmacology and experimental therapeutics, 369(3), 489-502 (2019-04-04)
Methionine deprivation induces growth arrest and death of cancer cells. To eliminate l-methionine we produced, purified, and characterized the recombinant pyridoxal 5'-phosphate (PLP)-dependent l-methionine γ-lyase (MGL)- BL929 from the cheese-ripening Brevibacterium aurantiacum Transformation of an Escherichia coli strain with the
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