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重组人p16-INK4a-TAT

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  • ¥1838
  • peprotech
  • USA
  • 110-02T
  • 2025年12月08日
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    上海研卉生物科技有限公司
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    • 详细信息
    • 文献和实验
    • 技术资料
    • 英文名：

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

    • 供应商：

      研卉生物

    • 规格：

      25ug

    重组人p16-INK4a-TAT（Recombinant Human p16-INK4a-TAT）
    别名：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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    相关实验

    • 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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