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Gene Review

Ids  -  iduronate 2-sulfatase

Rattus norvegicus

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Disease relevance of Ids


High impact information on Ids

  • The E1A mutants containing a deletion in either the N terminus or the conserved region 1 were unable to induce apoptosis in cooperation with Ids [2].
  • Apoptosis also is induced in mouse A40 (p53-/-) cells by E1A alone or E1A plus Ids after transient transfection of the expression vectors [2].
  • After induction of E1A and Ids, EId10 and EId23 cells began to accumulate in S phase and undergo apoptosis before entering G2 phase, suggesting that abnormal synthesis of DNA induced by coexpression of E1A, Id-1H, and Id-2H results in the induction of apoptosis [2].
  • Thus, Ids are localized to different cell types and are differentially expressed, at both the mRNA and protein levels, along the epididymis [3].
  • Uptake of recombinant iduronate-2-sulfatase into neuronal and glial cells in vitro [1].

Associations of Ids with chemical compounds

  • Two different approaches to obtain recombinant IDS have been utilized: production of the recombinant enzyme by a transfected human clone (Bosc 23 cells); production of the recombinant enzyme by adenoviral transduction of neuronal (SK-N-BE) or glial (C6) cells [1].
  • Our data indicate that the transfected as well as the infected cells produce a large amount of the IDS enzyme, which is efficiently endocytosed into neuronal and glial cells through the mannose 6-phosphate (M6P) receptor system [1].

Analytical, diagnostic and therapeutic context of Ids

  • The E1A domains required for induction of apoptosis, analysed by transfection with expression vectors for E1A, Ids and their mutants, followed by flow cytometry, reside in N-terminal (positions 17 - 38), CR1 and CR2 regions [4].
  • Somatic gene therapy appears therefore to be suitable to correct IDS deficiency in brain cells [1].


  1. Uptake of recombinant iduronate-2-sulfatase into neuronal and glial cells in vitro. Daniele, A., Tomanin, R., Villani, G.R., Zacchello, F., Scarpa, M., Di Natale, P. Biochim. Biophys. Acta (2002) [Pubmed]
  2. Suppression of adenovirus E1A-induced apoptosis by mutated p53 is overcome by coexpression with Id proteins. Nakajima, T., Yageta, M., Shiotsu, K., Morita, K., Suzuki, M., Tomooka, Y., Oda, K. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
  3. Expression, localization, and regulation of inhibitor of DNA binding (Id) proteins in the rat epididymis. Carroll, M., Hamzeh, M., Robaire, B. J. Androl. (2006) [Pubmed]
  4. The adenovirus E1A domains required for induction of DNA rereplication in G2/M arrested cells coincide with those required for apoptosis. Yageta, M., Tsunoda, H., Yamanaka, T., Nakajima, T., Tomooka, Y., Tsuchida, N., Oda, K. Oncogene (1999) [Pubmed]
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