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Anti-Human p16-INK4a-TAT

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  • ¥1725
  • PEPRO
  • 500-P284T
  • 2025年07月13日
  • wb elisa
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    • 文献和实验
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    • 抗体英文名

      Anti-Human p16-INK4a-TAT

    • 抗体名

      Anti-Human p16-INK4a-TAT

    • 规格

      50ug

    Anti-Human p16-INK4a-TAT
    Catalog Number:
    500-P284T
    Source:
    Polyclonal Rabbit
    Application:
    ELISA
    Sandwich
    To detect Human p16-INK4a-TAT by sandwich ELISA (using100μl/well antibody solution), a concentration of 0.5 - 2.0 μg/ml of this antibody is required. This antigen affinity purified antibody, in conjunction with PeproTech’s Biotinylated Anti-Human p16-INK4a-TAT (500-P284TBt) as a detection antibody, allows the detection of at least 0.2 - 0.4 ng/well of recombinant Human p16-INK4a-TAT.
    Western Blot
    To detect Human p16-INK4a-TAT by Western Blot analysis this antibody can be used at a concentration of 0.1 - 0.2 μg/ml.When used in conjunction with compatible secondary reagents, the detection limit for recombinant Human p16-INK4a-TAT is 1.5 - 3.0 ng/lane, under either reducing or non-reducing conditions. Western Blot:  500-P284T WB reducedWestern Blot:  500-P284T WB unreduced
    ProtocolItem/Western Transfer (Western Blot)
    Preparation:
    Produced from sera of rabbits immunized with highly pure recombinant Human p16-INK4a-TAT. Anti-Human p16-INK4a-TAT specific antibody was purified by affinity chromatography employing an immobilized Human p16-INK4a-TAT matrix.
    Immunogen:
    E.coli derived Recombinant Human p16-INK4a-TAT (PeproTech catalog #110-02T)
    Recombinant Human p16-INK4a-TAT
    Catalog Number:
    110-02T
    Synonyms:
    Cyclin-dependent kinase inhibitor 2A, Cyclin-dependent kinase 4 inhibitor A, CDK4I, p16INK4A, p16-INK4, Multiple tumor suppressor 1, MTS-1
    Description:
    p16-INK4a is a nuclear protein that regulates the cell cycle by inhibiting cyclin-dependent kinase-4 (CDK4) and CDK6. p16-INK4a 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. p16-INK4a and other transcription factors have been introduced into cells by DNA transfection, viral infection, or microinjection. Protein transduction using TAT fusion proteins represents an alternative methodology for introducing transcription factors and other nuclear proteins into primary, as well as transformed, cells. Recombinant Human p16-INK4a-TAT expressed in E. coli is an 18.0 kDa protein containing 167 amino-acid residues, including the 155 residues of full-length p16-INK4a and a 12-residue C-terminal TAT peptide (GYGRKKRRQRRR).

    AA Sequence:
    EPAAGSSMEP SADWLATAAA RGRVEEVRAL LEAGALPNAP NSYGRRPIQV MMMGSARVAE LLLLHGAEPN CADPATLTRP VHDAAREGFL DTLVVLHRAG ARLDVRDAWG RLPVDLAEEL GHRDVARYLR AAAGGTRGSN HARIDAAEGP SDIPDGYGRK KRRQRRR
    Source:
    E.coli
    Purity:
    Greater than 95% by SDS-PAGE gel and HPLC analyses.

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    图标文献和实验
    相关实验
    • p16INK4A and Familial Melanoma

      alterations affecting p16INK4A and cyclin D1 are so frequent in human cancers that inactivation of these proteins is believed to be necessary for tumor development. Broadly applicable anticancer therapies might be based on restoration of p16INK4A CDK

    • 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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