PIK3IP1 Proteins, cDNA Clones Research Reagents

PIK3IP1 (Phosphoinositide-3-Kinase Interacting Protein 1) is a protein coding gene located on human chromosome 22q12.2. PIK3IP1 is also known as HGFL, TrIP and hHGFL(S). The human PIK3IP1 gene encodes a 28248 Da protein containing 263 amino acids. The PIK3IP1 protein is ubiquitously expressed in lymph node, appendix and other tissues. PIK3IP1 is related to phosphatidylinositol 3-kinase catalytic subunit binding. MST1 is an important paralog of PIK3IP1 gene. PIK3IP1 is associated with Endometrioid Ovary Carcinoma.

PIK3IP1 Protein (2)

    PIK3IP1 cDNA Clone (14)


    In expression vector


    クローニングベクター cDNA 製品

    In lentiviral vector

    PIK3IP1 qPCR Primer (1)

    PIK3IP1 Lysate (2)

      PIK3IP1 の背景知識

      PIK3IP1 contains 1 kringle domain and is a negative regulator of phosphatidylinositol-3-kinase (PI3K), suppresses the development of hepatocellular carcinoma. PI3K is a well-known regulator of cell division, motility, metabolism and survival in most cell types. Proper liver function and development highly depend on intact PI3K signal transduction. Aberrant PI3K pathway signaling in the liver is associated with hepatocellular carcinoma. PI3K signaling is involved in the homeostasis of lipid and glucose metabolism. Activation of the PI3K pathway induces lipogenesis and glycogenesis in the liver, since both Akt overexpressing transgenic mice and PTEN knockout mice develop fatty liver and hypoglycemia. PIK3IP1 overexpression can contribute to glucose homeostasis and fatty deposition.

      PIK3IP1 の参考文献

      • He X, et al. (2008) PIK3IP1, a negative regulator of PI3K, suppresses the development of hepatocellular carcinoma. Cancer Res. 68(14):5591-8.
      • Gao P, et al. (2008) Both PIK3IP1 and its novel found splicing isoform, PIK3IP1-v1, are located on cell membrane and induce cell apoptosis. Beijing Da Xue Xue Bao. 40(6):572-7.
      • Zhu Z, et al. (2007) PI3K is negatively regulated by PIK3IP1, a novel p110 interacting protein. Biochem Biophys Res Commun. 358(1):66-72.

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