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Gene Review

ATL2  -  atlastin GTPase 2

Homo sapiens

Synonyms: ADP-ribosylation factor-like protein 6-interacting protein 2, ARL-6-interacting protein 2, ARL3IP2, ARL6IP2, Aip-2, ...
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Disease relevance of ARL6IP2

  • We have cloned three pairs of rearranged and germ-line variable region (V beta) genes of the beta chain of the human T-cell receptor from the cell lines ATL2, ATL12, and MT-1 of patients with adult T-cell leukemia (ATL) [1].
  • Using gel filtration, procion red Sepharose, DEAE, and reverse phase chromatography, we have purified ADF protein to homogeneity from 15 liters of serum-free culture supernatant of an HTLV-I(+) T cell line ATL-2 [2].
  • We demonstrated that while PB-1 cells are infectable by both X4 and R5 HIV, Sez-4, C91PL, HUT 102B and ATL-2 cells were infected by X4 HIV only [3].

High impact information on ARL6IP2

  • A neu protein-specific activating factor (NAF) was partially purified from medium conditioned by the transformed human T-cell line ATL-2 [4].
  • Recombinant ADF could sustain growth of 3B6 and ATL-2 cells at low cellular concentration without fetal calf serum; ADF, thus, appears involved in their autocrine growth [5].
  • Comparison of the nucleotide sequences showed no somatic mutation in V beta X ATL2 and beta X ATL12-2 [1].
  • 13cRA induced apoptosis in ATL2 cells within 48 h in a dose-dependent manner [6].
  • Because HTLV-I-infected lymphocytes are susceptible to oxidative stress, we examined the role of the intracellular redox state in 13cRA-induced cell death using a HTLV-I-positive T-cell line, ATL2, as a model [6].

Chemical compound and disease context of ARL6IP2

  • In this study, five single clones were randomly established by limiting dilution method from each of the HTLV-I positive T cell lines - HUT 102 and ATL-2, and examined for the all-trans retinoic acid (ATRA) sensitivity, respectively [7].

Biological context of ARL6IP2


Anatomical context of ARL6IP2

  • Unlike Tac Ag on HTLV(+), ATL-derived cell lines (Hut-102, MT-1, ATL-2), the expression of Tac Ag on YT cells was down-regulated by anti-Tac Ab [9].
  • Furthermore, recombinant ADF (rADF) and suboptimal dose of 2-ME additively enhanced the growth of ATL-2 cells in L-cystine-free medium, implying the possible involvement of endogenous reducing agents such as ADF/thioredoxin homologue in the process of lymphocyte transformation/activation [10].
  • ATL-2 CM dose-dependently inhibited hepatocyte proliferation [8].
  • No class II-re-expressed ATL-2 cells were observed in the SEB-presenting cultures by indirect immunofluorescence, and only minimum inhibition of SEB-dependent T-cell response by anti-human leukocyte antigen (HLA)-DR monoclonal antibody was observed [11].

Analytical, diagnostic and therapeutic context of ARL6IP2

  • Immunoblotting and sequential immunoprecipitation with these antibodies revealed the same 13-kDa protein in 3B6 and ATL-2 cells [5].
  • Among the cell lines derived from peripheral blood, HPB-ATL-T (ATL-T), HPB-ATL-2 (ATL-2) and HPB-ATL-O were more progressed than Tax exclusively expressing HPB-CTL-I (CTL-I), because the former deleted p16 gene (polymerase chain reaction (PCR)) and strongly transcribed survivin (reverse transcriptase-PCR) [11].


  1. Low frequency of somatic mutation in beta-chain variable region genes of human T-cell receptors. Ikuta, K., Ogura, T., Shimizu, A., Honjo, T. Proc. Natl. Acad. Sci. U.S.A. (1985) [Pubmed]
  2. IL-2 receptor(p55)/Tac-inducing factor. Purification and characterization of adult T cell leukemia-derived factor. Tagaya, Y., Okada, M., Sugie, K., Kasahara, T., Kondo, N., Hamuro, J., Matsushima, K., Dinarello, C.A., Yodoi, J. J. Immunol. (1988) [Pubmed]
  3. New T-lymphocytic cell lines for studying cell infectability by human immunodeficiency virus. Rozmyslowicz, T., Kijowski, J., Conover, D.O., Majka, M., Baj-Krzyworzeka, M., Reca, R., Libura, J.J., Gaulton, G.N., Ratajczak, M.Z. Eur. J. Haematol. (2001) [Pubmed]
  4. Characterization of a neu/c-erbB-2 protein-specific activating factor. Dobashi, K., Davis, J.G., Mikami, Y., Freeman, J.K., Hamuro, J., Greene, M.I. Proc. Natl. Acad. Sci. U.S.A. (1991) [Pubmed]
  5. Adult T-cell leukemia-derived factor/thioredoxin, produced by both human T-lymphotropic virus type I- and Epstein-Barr virus-transformed lymphocytes, acts as an autocrine growth factor and synergizes with interleukin 1 and interleukin 2. Wakasugi, N., Tagaya, Y., Wakasugi, H., Mitsui, A., Maeda, M., Yodoi, J., Tursz, T. Proc. Natl. Acad. Sci. U.S.A. (1990) [Pubmed]
  6. Role of intracellular redox status in apoptosis induction of human T-cell leukemia virus type I-infected lymphocytes by 13-cis-retinoic acid. Furuke, K., Sasada, T., Ueda-Taniguchi, Y., Yamauchi, A., Inamoto, T., Yamaoka, Y., Masutani, H., Yodoi, J. Cancer Res. (1997) [Pubmed]
  7. A mechanism of apoptosis induced by all-trans retinoic acid on adult T-cell leukemia cells: a possible involvement of the Tax/NF-kappaB signaling pathway. Nawata, H., Maeda, Y., Sumimoto, Y., Miyatake, J., Kanamaru, A. Leuk. Res. (2001) [Pubmed]
  8. Hepatocyte growth inhibitory factor derived from HTLV-I(+) T cell lines: effect on the epidermal growth factor-dependent proliferation of rat hepatocytes. Inamoto, T., Yamauchi, A., Nakamura, H., Nakamura, Y., Kanai, M., Maeda, M., Tagaya, Y., Yodoi, J., Ozawa, K. Clin. Immunol. Immunopathol. (1991) [Pubmed]
  9. TCGF (IL 2)-receptor inducing factor(s). I. Regulation of IL 2 receptor on a natural killer-like cell line (YT cells). Yodoi, J., Teshigawara, K., Nikaido, T., Fukui, K., Noma, T., Honjo, T., Takigawa, M., Sasaki, M., Minato, N., Tsudo, M. J. Immunol. (1985) [Pubmed]
  10. Lymphocyte transformation and thiol compounds; the role of ADF/thioredoxin as an endogenous reducing agent. Yamauchi, A., Masutani, H., Tagaya, Y., Wakasugi, N., Mitsui, A., Nakamura, H., Inamoto, T., Ozawa, K., Yodoi, J. Mol. Immunol. (1992) [Pubmed]
  11. Human leukocyte antigen-class II-negative long-term cultured human T-cell leukemia virus type-I-infected T-cell lines with progressed cytological properties significantly induce superantigen-dependent normal T-cell proliferation. Nagasaki, M., Zhang, J., Morikawa, S., Harada, T., Nabika, T., Tanaka, Y. Pathol. Int. (2005) [Pubmed]
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