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Gene Review

Kin  -  antigenic determinant of rec-A protein

Mus musculus

Synonyms: Binding to curved DNA, Btcd, DNA/RNA-binding protein KIN17, KIN, antigenic determinant of recA protein, Kin17
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Disease relevance of Kin


High impact information on Kin

  • In addition to having catalytic activity, the C alpha subunit from Kin- cells is inhibited in the presence of mouse RI alpha regulatory subunit, indicating that formation of the holoenzyme complex is normal [1].
  • We suggest that the mutation responsible for the Kin- phenotype is in a cellular component that directly or indirectly causes Kin- catalytic subunit protein to be degraded rapidly [1].
  • Poly(A+) RNA was isolated from Y1 and Kin mutant cells and was translated in a cell-free, reticulocyte lysate system in the presence of L-[35S]methionine [2].
  • A series of mutant cell lines (Kin) were previously isolated from Y1 adrenocortical tumor cells based on their ability to resist the growth-inhibitory effects of 8-bromo cAMP [3].
  • These observations indicate that the cAMP-resistant phenotype of Kin mutant clones resulted specifically from single mutational events in RI and thus establish the importance of cAMPdPK as an essential regulator of adrenocortical function [3].

Biological context of Kin

  • We cloned the C alpha cDNA from Kin- cells and show that its transient expression in another cell type leads to activation of a cAMP-sensitive luciferase reporter gene, suggesting that functional C alpha protein is made [1].
  • The -170 element was 25-fold more effective in enhancing gene expression from the reporter construct in Y1 cells than in Kin mutant cells; the elements at -65, -140, and -210 were 3-fold more effective in Y1 cells than in Kin mutant cells; the -280 element was equally effective in the parent and Kin mutant clones [4].
  • Expression of Kin, a nuclear protein binding to curved DNA, in mammal and avian brains [5].
  • In conclusion, the expression of the Kin protein is preserved in the phylogeny of the brain of higher vertebrates [5].
  • The distribution of Kin protein, the vertebrate homologue of the bacterial recA nuclear protein involved in illegitimate recombinant DNA repair and gene regulation, was analysed in the brain of the mouse, quail, turtle and frog by immunocytochemical methods [6].

Anatomical context of Kin


Associations of Kin with chemical compounds

  • Studies on the conversion of 22(R)-hydroxycholesterol into steroid products in parent and mutant cells indicate that the Kin mutations reduce the steroidogenic capacity of the cell as well as inhibit the hormone- and cyclic nucleotide-dependent mobilization of substrate cholesterol [8].
  • Molecular basis for the 3',5'-cyclic adenosine monophosphate resistance of Kin mutant Y1 adrenocortical tumor cells [3].
  • The Kin 8 cell line is derived from Y1 cells and harbours a defect in the cyclic AMP (cAMP)-dependent protein kinase, making it refractory to cAMP-dependent regulation of several enzymes [9].
  • Three different forms of glutathione transferase (GST) have been resolved in the two mouse adrenal tumour cell lines Y1 and Kin 8 [9].
  • C2 toxin treatment of a protein kinase A mutant Y-1 cell (Kin 8) resulted in morphological changes and an increase in steroid output that was not different from that observed for wild type Y-1 cells [10].

Other interactions of Kin

  • We demonstrate that although the Kin- cell line lacks detectable catalytic subunit protein, these cells express wild-type levels of mRNA for both C alpha and C beta catalytic subunit isoforms [1].
  • These results strongly support the hypothesis that impaired expression of steroidogenic enzymes in the Kin mutants results directly from defects in cAMP-dependent protein kinase activity [11].
  • Also, the steady-state levels of mGTmu1 mRNA were much lower in Y1 cells treated with forskolin (which activates adenylate cyclase) compared with control cells, but there was no difference in mGTmu1 mRNA levels between control and forskolin-treated Kin 8 cells [9].
  • Cytochalasin E also caused induction of plasminogen activation in Y1, but not in Kin 2 or Kin 8 cells [12].

Analytical, diagnostic and therapeutic context of Kin

  • Using immunocytochemistry with anti-RecA antibodies, we report the ubiquitous presence of the Kin protein in the CNS of mice and quails [5].


  1. The S49 Kin- cell line transcribes and translates a functional mRNA coding for the catalytic subunit of cAMP-dependent protein kinase. Orellana, S.A., McKnight, G.S. J. Biol. Chem. (1990) [Pubmed]
  2. mRNA from mutant Y1 adrenal cells directs the synthesis of altered regulatory subunits of type 1 cAMP-dependent protein kinase. Williams, S.A., Schimmer, B.P. J. Biol. Chem. (1983) [Pubmed]
  3. Molecular basis for the 3',5'-cyclic adenosine monophosphate resistance of Kin mutant Y1 adrenocortical tumor cells. Olson, M.F., Krolczyk, A.J., Gorman, K.B., Steinberg, R.A., Schimmer, B.P. Mol. Endocrinol. (1993) [Pubmed]
  4. Identification of promoter elements in the mouse 21-hydroxylase (Cyp21) gene that require a functional cyclic adenosine 3',5'-monophosphate-dependent protein kinase. Parissenti, A.M., Parker, K.L., Schimmer, B.P. Mol. Endocrinol. (1993) [Pubmed]
  5. Expression of Kin, a nuclear protein binding to curved DNA, in mammal and avian brains. Mermet, N., Angulo, J., Repérant, J., Medina, M., Araneda, S. Neurosci. Lett. (1998) [Pubmed]
  6. Expression of Kin, a nuclear protein binding to curved DNA, in the brain of the frog (Rana esculenta), turtle (Trachemys scripta), quail (Coturnix coturnix) and mouse (Mus musculus). Mermet, N., Angulo, J., Médina, M., Repérant, J., Ward, R., Araneda, S. Anat. Embryol. (2002) [Pubmed]
  7. Permeability of the blood-brain barrier to the immunosuppressive cyclic peptide cyclosporin A. Begley, D.J., Squires, L.K., Zloković, B.V., Mitrović, D.M., Hughes, C.C., Revest, P.A., Greenwood, J. J. Neurochem. (1990) [Pubmed]
  8. The causal relationship between mutations in cAMP-dependent protein kinase and the loss of adrenocorticotropin-regulated adrenocortical functions. Wong, M., Krolczyk, A.J., Schimmer, B.P. Mol. Endocrinol. (1992) [Pubmed]
  9. Adrenocorticotrophic-hormone-dependent regulation of a mu-class glutathione transferase in mouse adrenocortical cells. Mankowitz, L., Staffas, L., Bakke, M., Lund, J. Biochem. J. (1995) [Pubmed]
  10. Botulinum C2 toxin and steroid production in adrenal Y-1 cells: the role of microfilaments in the toxin-induced increase in steroid release. Considine, R.V., Simpson, L.L., Sherwin, J.R. J. Pharmacol. Exp. Ther. (1992) [Pubmed]
  11. The roles of cAMP and cAMP-dependent protein kinase in the expression of cholesterol side chain cleavage and steroid 11 beta-hydroxylase genes in mouse adrenocortical tumor cells. Wong, M., Rice, D.A., Parker, K.L., Schimmer, B.P. J. Biol. Chem. (1989) [Pubmed]
  12. Action of 12-O-tetradecanoylphorbol-13-acetate on Y1 adrenal cells apparently requires the regulatory subunit of type 1 cyclic AMP dependent protein kinase. Estensen, R.D., Zustiak, K., Chuang, A., Schultheiss, P., Ditmanson, J. J. Exp. Pathol. (1983) [Pubmed]
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