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Titolo:
Alymphoplasia is caused by a point mutation in the mouse gene encoding Nf-kappa b-inducing kinase
Autore:
Shinkura, R; Kitada, K; Matsuda, F; Tashiro, K; Ikuta, K; Suzuki, M; Kogishi, K; Serikawa, T; Honjo, T;
Indirizzi:
Kyoto Univ, Grad Sch Med, Dept Med Chem, Sakyo Ku, Kyoto 6068501, Japan Kyoto Univ Kyoto Japan 6068501 Med Chem, Sakyo Ku, Kyoto 6068501, Japan Kyoto Univ, Grad Sch Med, Inst Lab Anim, Sakyo Ku, Kyoto 6068501, Japan Kyoto Univ Kyoto Japan 6068501 Lab Anim, Sakyo Ku, Kyoto 6068501, Japan Kyotopaniv, Grad Sch Med, Ctr Mol Biol & Genet, Sakyo Ku, Kyoto 6068501, Ja Kyoto Univ Kyoto Japan 6068501 Biol & Genet, Sakyo Ku, Kyoto 6068501, Ja Kumamoto Univ, Ctr Anim Resources & Dev, Kumamoto 8620976, Japan Kumamoto Univ Kumamoto Japan 8620976 rces & Dev, Kumamoto 8620976, Japan
Titolo Testata:
NATURE GENETICS
fascicolo: 1, volume: 22, anno: 1999,
pagine: 74 - 77
SICI:
1061-4036(199905)22:1<74:AICBAP>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
LYMPHOTOXIN-BETA-RECEPTOR; TUMOR-NECROSIS-FACTOR; PERIPHERAL LYMPHOID ORGANS; ALY MUTANT MICE; DEFICIENT MICE; CELL-DEATH; ALPHA; ORGANOGENESIS; ORGANIZATION; EXPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Honjo, T Kyoto Univ, Grad Sch Med, Dept Med Chem, Sakyo Ku, Kyoto 6068501,Japan Kyoto Univ Kyoto Japan 6068501 , Sakyo Ku, Kyoto 6068501, Japan
Citazione:
R. Shinkura et al., "Alymphoplasia is caused by a point mutation in the mouse gene encoding Nf-kappa b-inducing kinase", NAT GENET, 22(1), 1999, pp. 74-77

Abstract

The alymphoplasia (aly) mutation of mouse is autosomal recessive and characterized by the systemic absence of lymph nodes (LN) and Peyer's patches (PP) and disorganized splenic and thymic structures with immunodeficiency(1-3). Although recent reports have shown that the interaction between lymphotoxin (LT) and the LT beta-receptor (Lt beta r, encoded by Ltbr) provides a critical signal for LN genesis in mice(4-10), the aly locus on chromosome 11(ref, 11) is distinct from those for LT and its receptor. We found that the aly allele carries a point mutation causing an amino acid substitution inthe carboxy-terminal interaction domain of Nf-kappa b-inducing kinase(12,13) (Nik, encoded by the gene Nik). Transgenic complementation with wild-type Nik restored the normal structures of LN, PP, spleen and thymus, and the normal immune response in aly/aly mice. In addition, the aly mutation in a kinase domain-truncated Nik abolished its dominant-negative effect on Nf-kappa b activation induced by an excess of Lt beta r. Our observations agree with previous reports that Lt beta r-deficient mice showed defects in LN genesis(4) and that Nik is a common mediator of Nf-kappa b activation by the tumour necrosis factor (TNF) receptor family(12,13). Nik is able to interact with members of the TRAF family (Traf1, 2, 3, 5 and 6; ref. 13), suggesting it acts downstream of TRAF-associating receptor signalling pathways, including Tnfr (ref. 12), Cd40 (refs 14,15), Cd30 (refs 16,17) and Lt beta r (refs 18-21). The phenotypes of aly/aly mice are more severe than those of Ltbr(-/-) mice, however, indicating involvement of Nik in signal transduction mediated by other receptors.

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Documento generato il 25/01/20 alle ore 16:34:33