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Protein KIAA1199 is a protein that in humans is encoded by the KIAA1199 gene and has been associated with hearing loss.[1][2][3]


  1. Abe S, Usami S, Nakamura Y (Nov 2003). Mutations in the gene encoding KIAA1199 protein, an inner-ear protein expressed in Deiters' cells and the fibrocytes, as the cause of nonsyndromic hearing loss. J Hum Genet 48 (11): 564-70.
  2. Michishita E, Garces G, Barrett JC, Horikawa I (Jul 2006). Upregulation of the KIAA1199 gene is associated with cellular mortality. Cancer Lett 239 (1): 71-7.
  3. Entrez Gene: KIAA1199 KIAA1199.

Further readingEdit

  • Nagase T, Ishikawa K, Kikuno R, et al. (2000). Prediction of the coding sequences of unidentified human genes. XV. The complete sequences of 100 new cDNA clones from brain which code for large proteins in vitro.. DNA Res. 6 (5): 337–45.
  • Wines ME, Lee L, Katari MS, et al. (2001). Identification of mesoderm development (mesd) candidate genes by comparative mapping and genome sequence analysis.. Genomics 72 (1): 88–98.
  • Nakayama M, Kikuno R, Ohara O (2003). Protein-protein interactions between large proteins: two-hybrid screening using a functionally classified library composed of long cDNAs.. Genome Res. 12 (11): 1773–84.
  • Abe S, Katagiri T, Saito-Hisaminato A, et al. (2003). Identification of CRYM as a candidate responsible for nonsyndromic deafness, through cDNA microarray analysis of human cochlear and vestibular tissues.. Am. J. Hum. Genet. 72 (1): 73–82.
  • Strausberg RL, Feingold EA, Grouse LH, et al. (2003). Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences.. Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903.
  • Gerhard DS, Wagner L, Feingold EA, et al. (2004). The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).. Genome Res. 14 (10B): 2121–7.
  • Guo J, Cheng H, Zhao S, Yu L (2006). GG: a domain involved in phage LTF apparatus and implicated in human MEB and non-syndromic hearing loss diseases.. FEBS Lett. 580 (2): 581–4.

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