Human TBC1D4 peptide (ab23116)

関連情報

• 別名
  • Acrg embryonic lethality (mouse) minimal region ortholog
  • Acrg embryonic lethality minimal region ortholog
  • Acrg embryonic lethality mouse minimal region ortholog

  • Akt substrate of 160 kDa
  • AS 160
  • AS160
  • BUB2
  • CDC16
  • KIAA0603
  • NIDDM5
  • TBC (Tre 2 BUB2 CDC16) domain containing protein
  • TBC Tre 2 BUB2 CDC16 domain containing protein
  • TBC1 D4
  • TBC1 domain family member 4
  • Tbc1d4
  • TBCD4_HUMAN
  • Tre-2

  see all
• 機能May act as a GTPase-activating protein for RAB2A, RAB8A, RAB10 and RAB14. Isoform 2 promotes insulin-induced glucose transporter SLC2A4/GLUT4 translocation at the plasma membrane, thus increasing glucose uptake.
• 組織特異性Widely expressed. Isoform 2 is the highest overexpressed in most tissues. Isoform 1 is highly expressed in skeletal muscle and heart, but was not detectable in the liver nor in adipose tissue. Isoform 2 is strongly expressed in adrenal and thyroid gland, and also in lung, kidney, colon, brain and adipose tissue. Isoform 2 is moderately expressed in skeletal muscle. Expressed in pancreatic Langerhans islets, including beta cells (at protein level). Expression is decreased by twofold in pancreatic islets in type 2 diabetes patients compared to control subjects. Up-regulated in T cells from patients with atopic dermatitis.
• 配列類似性Contains 2 PID domains.
  Contains 1 Rab-GAP TBC domain.
• 翻訳後修飾Phosphorylated by AKT1; insulin-induced.
  Insulin-stimulated phosphorylation is required for SLC2A4/GLUT4 translocation.
  Physiological hyperinsulinemia increases phosphorylation in skeletal muscle. Insulin-stimulated phosphorylation is reduced by 39% in type 2 diabetic patients.
• 細胞内局在Cytoplasm. Isoform 2 shows a cytoplasmic perinuclear localization in a myoblastic cell line in resting and insulin-stimulated cells.

• Target information above from: UniProt accession O60343 The UniProt Consortium
  The Universal Protein Resource (UniProt) in 2010
  Nucleic Acids Res. 38:D142-D148 (2010) .

  Information by UniProt