Lyophilized from 5% (v/v) acetonitrile/H₂O. Reconstitute pellet in 200μl distilled water to obtain a 0.5mg/ml peptide solution.
Store as concentrated solution. Centrifuge briefly prior to opening vial. For short-term storage (1-2 weeks), store at 4ºC. For long-term storage, aliquot and store at -20ºC or below. Avoid multiple freeze-thaw cycles.
For laboratory use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
MLM blocking peptide , P16INK4 blocking peptide , P14ARF blocking peptide , CMM2 blocking peptide , CDKN2A blocking peptide , P16 blocking peptide , TP16 blocking peptide , CDKN2 blocking peptide , P14 blocking peptide , P19ARF blocking peptide , ARF blocking peptide , INK4A blocking peptide , INK4 blocking peptide , P16INK4A blocking peptide , CDK4I blocking peptide , MTS1 blocking peptide , P19 blocking peptide
This gene generates several transcript variants which differ in their first exons. At least three alternatively spliced variants encoding distinct proteins have been reported, two of which encode structurally related isoforms known to function as inhibitors of CDK4 kinase. The remaining transcript includes an alternate first exon located 20 Kb upstream of the remainder of the gene; this transcript contains an alternate open reading frame (ARF) that specifies a protein which is structurally unrelated to the products of the other variants. This ARF product functions as a stabilizer of the tumor suppressor protein p53 as it can interact with, and sequester, the E3 ubiquitin-protein ligase MDM2, a protein responsible for the degradation of p53. In spite of the structural and functional differences, the CDK inhibitor isoforms and the ARF product encoded by this gene, through the regulatory roles of CDK4 and p53 in cell cycle G1 progression, share a common functionality in cell cycle G1 control. This gene is frequently mutated or deleted in a wide variety of tumors, and is known to be an important tumor suppressor gene. [provided by RefSeq, Sep 2012]