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Key Documents

SRP3134

Sigma-Aldrich

p16-INK-4a

recombinant, expressed in E. coli, lyophilized, ≥95% (SDS-PAGE), ≥95% (HPLC), suitable for mammalian cell culture

Sinónimos:

CDK4I, Cyclin-dependent kinase 4 inhibitor A, Cyclin-dependent kinase inhibitor 2A, Multiple tumor suppressor 1, p16-INK4, p16INK4A

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About This Item

UNSPSC Code:
12352202
NACRES:
NA.32

product name

p16-INK-4a human, recombinant, expressed in E. coli, ≥95% (SDS-PAGE), ≥95% (HPLC), suitable for cell culture

biological source

human

recombinant

expressed in E. coli

assay

≥95% (HPLC)
≥95% (SDS-PAGE)

form

lyophilized

mol wt

16.5 kDa

packaging

pkg of 20 μg

technique(s)

cell culture | mammalian: suitable

impurities

<0.1 EU/μg endotoxin, tested

color

off-white to yellow

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

Gene Information

human ... CDKN2A(1029)

General description

p16-INK4a, which is also known as cyclin dependent kinase inhibitor 2A (CDKN2A), is a nuclear protein. The gene encoding this protein is localized on human chromosome 9p21, with three exons. Recombinant p16-INK4a is a 16.5kDa protein containing 156 amino acid residues.

Biochem/physiol Actions

Cyclin dependent kinase inhibitor 2A (CDKN2A) or p16-INK4a regulates the cell cycle by inhibiting cyclin dependent kinase-4 (CDK4) and CDK6. It inhibits CDK activity by binding to the CDK molecules in a manner that interferes with their ability to interact with cyclin D. This activity has the effect of suppressing tumor formation and growth, and of inducing replicative senescence in various normal cells, including stem cells. The expression of p16-INK4a steadily increases with age and tends to accumulate in stem cell compartments. The deletion, rearrangement, or mutation of the p16-INK4a gene is frequently found in melanomas as well as in certain other types of cancer. The protein is downregulated in bladder cancer.

Sequence

MEPAAGSSME PSADWLATAA ARGRVEEVRA LLEAGALPNA PNSYGRRPIQ VMMMGSARVA ELLLLHGAEP NCADPATLTR PVHDAAREGF LDTLVVLHRA GARLDVRDAW GRLPVDLAEE LGHRDVARYL RAAAGGTRGS NHARIDAAEG PSDIPD

Physical form

Lyophilized from 1 x PBS + 1.0 mM DTT, pH 7.2.

Reconstitution

Centrifuge the vial prior to opening. Reconstitute in water to a concentration of 0.1-1.0 mg/ml. Do not vortex. This solution can be stored at 2-8°C for up to 1 week. For extended storage, it is recommended to further dilute in a buffer containing a carrier protein (example 0.1% BSA) and store in working aliquots at -20°C to -80°C.

pictograms

Exclamation mark

signalword

Warning

hcodes

Hazard Classifications

Eye Irrit. 2

Storage Class

13 - Non Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Visite la Librería de documentos

Prognostic and Clinicopathological Significance of Downregulated p16 Expression in Patients with Bladder Cancer: A Systematic Review and Meta-Analysis.
Gan X
Disease Markers, 5259602-5259602 (2016)
Prevalence of p16 and CDK4 germline mutations in 48 melanoma-prone families in France. The French Familial Melanoma Study Group.
Soufir N
Human Molecular Genetics, 7(2), 209-216 (1998)
Immunohistological Expression of p16INK4a is Commonly Present Both in Benign and Malignant Sweat Gland Neoplasias.
Tsujita J
Fukuoka Igaku Zasshi = Hukuoka Acta Medica, 106(12), 323-329 (2015)
Jinsuke Nishino et al.
Cell, 135(2), 227-239 (2008-10-30)
Stem cells persist throughout life in diverse tissues by undergoing self-renewing divisions. Self-renewal capacity declines with age, partly because of increasing expression of the tumor suppressor p16(Ink4a). We discovered that the Hmga2 transcriptional regulator is highly expressed in fetal neural
A Okamoto et al.
Proceedings of the National Academy of Sciences of the United States of America, 91(23), 11045-11049 (1994-11-08)
Cell cycle arrest at the G1 checkpoint allows completion of critical macromolecular events prior to S phase. Regulators of the G1 checkpoint include an inhibitor of cyclin-dependent kinase, p16INK4; two tumor-suppressor proteins, p53 and RB (the product of the retinoblastoma-susceptibility

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