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Gene Review

Lect1  -  leukocyte cell derived chemotaxin 1

Rattus norvegicus

Synonyms: Chmi, Leukocyte cell-derived chemotaxin 1
 
 
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Disease relevance of Lect1

  • CONCLUSION: In experimental uremia, expansion of growth cartilage does not result from increased or persistent expression of ChM-I or from reduced VEGF expression at the cartilage-metaphyseal bone interphase [1].
  • Expression of the cartilage derived anti-angiogenic factor chondromodulin-I decreases in the early stage of experimental osteoarthritis [2].
 

High impact information on Lect1

  • Chondromodulin-I expression in the growth plate of young uremic rats [1].
  • A similar number of chondrocytes per column was positive for ChM-I in the 4 groups [1].
  • In accordance with the elongation of the hypertrophic stratum in uremia, the distance (X+/-SEM, microm) between the extracellular ChM-I signal and the metaphyseal end of growth cartilage was higher (P < 0.003) in UREM (236 +/- 40) and UREM-GH (297 +/- 17) than in SAL (92 +/- 7) and SPF (113 +/- 6) [1].
  • The effect of recombinant ChM-I on tube morphogenesis of retinal endothelial cells was examined in culture [3].
  • Immunoreactive ChM-I was present in these cells and also in the vitreous body [3].
 

Biological context of Lect1

  • The rat ChM-I gene was determined to encode the open reading frame of 334 amino acid residues, and ChM-I mRNA was exclusively expressed in cartilage, eye, and cerebellum in rats [3].
  • OBJECTIVE: Chondromodulin-I (ChM-I), a cartilage derived anti-angiogenic factor, has been shown to regulate the vascular invasion during endochondral bone formation [2].
 

Anatomical context of Lect1

 

Other interactions of Lect1

 

Analytical, diagnostic and therapeutic context of Lect1

  • METHODS: Growth cartilage ChM-I expression was investigated by immunohistochemistry, in situ hybridization, and reverse transcription-polymerase chain reaction (RT-PCR) in growth-retarded young uremic rats (UREM), control rats, fed ad libitum (SAL) or pair-fed with the UREM group (SPF), and uremic rats treated with growth hormone (UREM-GH) [1].
  • No differences in ChM-I expression were appreciated by RT-PCR [1].
  • Expression and localization of ChM-I in rat eyes were examined by RNase protection assay and in situ hybridization and by immunostaining, using an antibody against a synthetic peptide [3].

References

  1. Chondromodulin-I expression in the growth plate of young uremic rats. Amil, B., Fernandez-Fuente, M., Molinos, I., Rodriguez, J., Carbajo-Pérez, E., Garcia, E., Yamamoto, T., Santos, F. Kidney Int. (2004) [Pubmed]
  2. Expression of the cartilage derived anti-angiogenic factor chondromodulin-I decreases in the early stage of experimental osteoarthritis. Hayami, T., Funaki, H., Yaoeda, K., Mitui, K., Yamagiwa, H., Tokunaga, K., Hatano, H., Kondo, J., Hiraki, Y., Yamamoto, T., Duong, l.e. .T., Endo, N. J. Rheumatol. (2003) [Pubmed]
  3. Expression and localization of angiogenic inhibitory factor, chondromodulin-I, in adult rat eye. Funaki, H., Sawaguchi, S., Yaoeda, K., Koyama, Y., Yaoita, E., Funaki, S., Shirakashi, M., Oshima, Y., Shukunami, C., Hiraki, Y., Abe, H., Yamamoto, T. Invest. Ophthalmol. Vis. Sci. (2001) [Pubmed]
  4. Chondromodulin-I expression in rat articular cartilage. Kitahara, H., Hayami, T., Tokunaga, K., Endo, N., Funaki, H., Yoshida, Y., Yaoita, E., Yamamoto, T. Arch. Histol. Cytol. (2003) [Pubmed]
  5. Localization and expression of chondromodulin-I in the rat cornea. Fukushima, A., Funaki, H., Yaoeda, K., Tanaka, T., Shirakashi, M., Yoshida, Y., Yaoita, E., Abe, H., Yamamoto, T. Arch. Histol. Cytol. (2003) [Pubmed]
 
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