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CDK6-Knockdown HeLa Cell Lysate

价格 3,600.00 1-2周
货号 S0Y0004
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产品规格
  • 宿主来源

    Human
  • 突变

    Mutation in exon1
  • 浓度

    2 mg/ml
  • 性状

    Liquid
  • 缓冲体系

    Supplied in SDS Sample Buffer: 50 mM Tris-HCl (pH 6.8 at 25°C), 2% w/v SDS, 10% glycerol, 1% v/v β-Mercaptoethanol, 0.01% w/v bromophenol blue or phenol red.

  • 储存条件

    -20 °C for 1 months under sterile conditions;
    -80 °C for 24 months under sterile conditions.
    Please avoid repeated freeze-thaw cycles.

  • 产品详情

    CDK6-Knockdown HeLa Cell Lysate is a lysate derived from a polyclonal population of HeLa cells in which CDK6 expression has been knocked down using CRISPR/Cas9 gene editing. The knockdown efficiency has been confirmed by Western blot, and the targeted mutation is located within exon 1 of the CDK6 gene. A control lysate from non-targeting HeLa cells is included for comparison.
    Key Notes:
    Boil for 3~5 minutes prior to use.
    Prepared from cells lysed in RIPA buffer (supplemented with protease and phosphatase inhibitors).
    Positive Control: CDK6-knockdown HeLa cell lysate supplied in SDS sample buffer with bromophenol blue.
    Negative Control: Control HeLa cell lysate supplied in SDS sample buffer with phenol red.

  • 应用

    WB

背景介绍
  • CDK6 (cyclin-dependent kinase 6) is a protein kinase involved in cell cycle regulation, with a molecular weight of approximately 40 kDa. CDK6 is expressed in various tissues including lymphoid tissues and the brain. It is activated by binding to D-type cyclins, and its core function is to phosphorylate the retinoblastoma protein, thereby relieving its block on the cell cycle and driving the transition from the G1 phase to the S phase. In addition to this classic role in promoting cell cycle progression, CDK6 also regulates processes such as cell differentiation and apoptosis by phosphorylating other substrates. Due to its dysregulated activity being closely associated with various cancers, CDK6 has become an important anticancer target. CDK4/6 inhibitors targeting it have been successfully applied in clinical practice, but resistance mechanisms such as CDK6 protein overexpression remain a major challenge in current treatment.

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