PLA0178
Rabbit anti-p16INK4a Antibody, Affinity Purified
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Synonym(s):
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
UNSPSC Code:
12352203
NACRES:
NA.41
Recommended Products
biological source
rabbit
Quality Level
antibody form
affinity purified immunoglobulin
antibody product type
primary antibodies
grade
Powered by Bethyl Laboratories, Inc.
species reactivity
human
concentration
0.2 mg/mL
technique(s)
immunohistochemistry: 1:100-1:500
immunoprecipitation (IP): 2-10 μg/mg
western blot: 1:2,000- 1:10,000
accession no.
AAA92554.1
shipped in
wet ice
storage temp.
2-8°C
target post-translational modification
unmodified
Gene Information
rabbit ... p16INK4a(1029)
General description
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) .
Immunogen
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).
Biochem/physiol Actions
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.
Physical form
Tris-buffered Saline containing 0.1% BSA containing 0.09% Sodium Azide
Other Notes
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.
Disclaimer
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.
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
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Certificates of Analysis (COA)
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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
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)
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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