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Gene Review

Cd47  -  Cd47 molecule

Rattus norvegicus

Synonyms: IAP, Integrin-associated protein, Leukocyte surface antigen CD47
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Disease relevance of Cd47

  • We generated a recombinant adenovirus vector expressing a neuronal form of CD47/IAP, and found that the expression of CD47/IAP by infection with CD47/IAP adenovirus induced the death of cultured cerebral cortical neurons [1].
  • This QA/Glu reaction is inhibited by islet-activating protein (IAP, pertussis toxin), but was not blocked by Joro spider toxin (JSTX), a specific blocker of traditional ionotropic QA/Glu receptors [2].
  • Islet-activating protein (IAP, a Bordetella pertussis toxin) was employed to test the hypothesis that the inhibitory GTP-binding regulatory protein of adenylate cyclase (Ni) mediates GTP effects on the binding of Ca2+-mobilizing hormones to liver plasma membranes and is involved in calcium mobilization stimulated by these agonists [3].
  • In hypercapnia, rCBF increased by 100% and 37% in the HIPDm (n = 5) and IAP (n = 5) groups, respectively [4].
  • In hypocapnia, IAP rCBF (n = 4) decreased 34% but HIPDm rCBF (n = 4) did not change [4].

Psychiatry related information on Cd47


High impact information on Cd47

  • Cleaved products of poly(ADP-ribose) polymerase 1 were elevated by ER (P < 0.025) providing biochemical evidence of apoptosis induction. cDNA microarray analysis identified the Bcl-2, CARD, and IAP functional gene groupings as being involved in apoptosis induction [6].
  • Three cDNA fragments corresponding to different spliced forms of integrin-associated protein (IAP) mRNA were found to be differentially expressed in the hippocampus of good-memory rats [7].
  • The IAP mRNA expression was significantly upregulated by NMDA and amphetamine injections to the dentate gyrus of the hippocampus [7].
  • On the other hand, injection of antisense oligonucleotide complementary to the IAP transcript markedly impaired memory retention in rats and decreased the amplitude and slope of EPSP in the in vivo long-term potentiation paradigm [7].
  • After down-regulation of the endogenous IAP by small interfering RNA, MAPK activity, synaptic protein levels, and glutamate release decreased [8].

Chemical compound and disease context of Cd47

  • 5. Pertussis toxin (IAP) treatment did not block the facilitatory effect of 5-HT on IGly [9].
  • Pretreatment of cultures from both ages by Bordetella pertussis toxin (IAP) was found to eliminate any Gpp(NH)p effect on carbamylcholine binding [10].
  • The mGlu response was abolished by pretreatment with either caffeine or ryanodine, but treatment with pertussis toxin (IAP) for 6-8 h had no effect [11].
  • We compared the effects of guanine nucleotides and Mg2+ on ADP-ribosylation of rat brain and liver membrane proteins catalysed by Bordetella pertussis toxin (IAP) and cholera toxin (CT) [12].
  • Intracellular application of either guanosine 5'-O-(2-thiodiphosphate) (GDP-betaS) or pertussis toxin (IAP) suppressed I(DA) [13].

Biological context of Cd47

  • These results suggest that CD47/IAP is involved in a novel pathway which regulates caspase-dependent apoptosis of cultured cerebral cortical neurons [1].
  • These results together suggest that IAP gene expression plays an important role in memory formation and synaptic plasticity in rat hippocampus [7].
  • These observations suggest that the IAP plays important roles in dendritic outgrowth and synaptic transmission in developing cortical neurons through the activation of MAPK [8].
  • Guanosine 5'-(3-O-thio)triphosphate or IAP treatment reduced the number of the high-affinity state binding sites without altering the KD for PIA [14].
  • These alkylations resulted in loss of its ability to be ADP-ribosylated by IAP and to associate with beta gamma, but leaving the GTP-binding site of alpha o intact [15].

Anatomical context of Cd47


Associations of Cd47 with chemical compounds

  • Group 3 including PIA and AMP did not affect phospholipase C, but inhibited the ANP performance in an IAP-sensitive fashion [17].
  • Group 2 including GTP and 8-bromoadenosine 5'-triphosphate acted similarly to Group 1 except for total insensitivity of the former to IAP [17].
  • The IAP-insensitive portion of Group 1 actions and the actions of Group 2 as well as of A23187, a Ca2+ ionophore which mimicked the Group 2 agonist actions, were almost completely inhibited by phosphodiesterase inhibitors such as M & B 22948 (2-O-propoxyphenyl-8-azapurin-6-one) and 3-isobutyl-1-methylxanthine [17].
  • However, IAP treatment decreased [3H]angiotensin II binding affinity when studies were performed in the absence but not the presence of 5'-guanylylimidodiphosphate (GppNHp) [3].
  • Angiotensin II attenuated glucagon-stimulated increases in cAMP in hepatocytes prepared from control but not IAP-treated rats [3].

Other interactions of Cd47


Analytical, diagnostic and therapeutic context of Cd47

  • The cerebral uptake of [99mTc]-d,l-hexamethylpropyleneamine oxime complex (HM-PAO) was compared to LCBF determined simultaneously with [14C]iodoantipyrine (IAP) using double radionuclide quantitative digital autoradiography [19].
  • Regional HM-PAO concentration was found not to be linearly related to LCBF as determined with the IAP, and therefore a simple microsphere type model was inadequate in relating HM-PAO uptake to LCBF [19].
  • Awake male rats were given intravenous injections of a mixture of 50 microCi IAP and 15 mCi of HM-PAO and killed 20 s after tracer activity had first reached the brain [19].
  • RESULTS: In the area at risk, regional myocardial blood flow (rMBF) evaluated by IAP recovered to the level in the nonischemic septum in all hearts, except in 60-min occlusion without reperfusion [20].
  • Because of the minute amount of IAP present in the brain, we have adopted the quantitative reverse transcription-polymerase chain reaction (RT-PCR) method [5].


  1. Expression of CD47/integrin-associated protein induces death of cultured cerebral cortical neurons. Koshimizu, H., Araki, T., Takai, S., Yokomaku, D., Ishikawa, Y., Kubota, M., Sano, S., Hatanaka, H., Yamada, M. J. Neurochem. (2002) [Pubmed]
  2. A new type of glutamate receptor linked to inositol phospholipid metabolism. Sugiyama, H., Ito, I., Hirono, C. Nature (1987) [Pubmed]
  3. Effect of islet-activating pertussis toxin on the binding characteristics of Ca2+-mobilizing hormones and on agonist activation of phosphorylase in hepatocytes. Lynch, C.J., Prpic, V., Blackmore, P.F., Exton, J.H. Mol. Pharmacol. (1986) [Pubmed]
  4. Comparison of [125I]HIPDm and [125I]iodoantipyrine in quantifying regional cerebral blood flow in rats. Albright, R.E., Friedman, A.H., Fram, E.K., Harbury, O.L., Molter, B.A., Skatoff, J.H., Harris, C.C., Coleman, R.E., Drayer, B.P. Stroke (1988) [Pubmed]
  5. Induction of integrin-associated protein (IAP) mRNA expression during memory consolidation in rat hippocampus. Lee, E.H., Hsieh, Y.P., Yang, C.L., Tsai, K.J., Liu, C.H. Eur. J. Neurosci. (2000) [Pubmed]
  6. Identification of the apoptosis activation cascade induced in mammary carcinomas by energy restriction. Thompson, H.J., Zhu, Z., Jiang, W. Cancer Res. (2004) [Pubmed]
  7. Expression of integrin-associated protein gene associated with memory formation in rats. Huang, A.M., Wang, H.L., Tang, Y.P., Lee, E.H. J. Neurosci. (1998) [Pubmed]
  8. Neuronal roles of the integrin-associated protein (IAP/CD47) in developing cortical neurons. Numakawa, T., Ishimoto, T., Suzuki, S., Numakawa, Y., Adachi, N., Matsumoto, T., Yokomaku, D., Koshimizu, H., Fujimori, K.E., Hashimoto, R., Taguchi, T., Kunugi, H. J. Biol. Chem. (2004) [Pubmed]
  9. Protein kinase C-mediated enhancement of glycine response in rat sacral dorsal commissural neurones by serotonin. Xu, T.L., Nabekura, J., Akaike, N. J. Physiol. (Lond.) (1996) [Pubmed]
  10. Guanosine 5'-triphosphate binding protein (Gi) and two additional pertussis toxin substrates associated with muscarinic receptors in rat heart myocytes: characterization and age dependency. Moscona-Amir, E., Henis, Y.I., Sokolovsky, M. Biochemistry (1988) [Pubmed]
  11. Metabotropic glutamate response in acutely dissociated hippocampal CA1 pyramidal neurones of the rat. Shirasaki, T., Harata, N., Akaike, N. J. Physiol. (Lond.) (1994) [Pubmed]
  12. Pertussis toxin substrate is a guanosine 5'-[beta-thio]diphosphate-, N-ethylmaleimide-, Mg2+- and temperature-sensitive GTP-binding protein. Wong, S.K., Martin, B.R., Tolkovsky, A.M. Biochem. J. (1985) [Pubmed]
  13. Dopamine activates inward rectifier K+ channel in acutely dissociated rat substantia nigra neurones. Uchida, S., Akaike, N., Nabekura, J. Neuropharmacology (2000) [Pubmed]
  14. Possible involvement of pertussis toxin-sensitive G proteins and D2 dopamine receptors in the A1 adenosine receptor-adenylate cyclase system in rat cerebral cortex. Murayama, T., Itahashi, Y., Nomura, Y. J. Neurochem. (1990) [Pubmed]
  15. Identification of sites for alkylation by N-ethylmaleimide and pertussis toxin-catalyzed ADP-ribosylation on GTP-binding proteins. Hoshino, S., Kikkawa, S., Takahashi, K., Itoh, H., Kaziro, Y., Kawasaki, H., Suzuki, K., Katada, T., Ui, M. FEBS Lett. (1990) [Pubmed]
  16. Evaluation of [123I]isopropyliodoamphetamine as a tracer for local cerebral blood flow using direct autoradiographic comparison. Lear, J.L., Ackermann, R.F., Kameyama, M., Kuhl, D.E. J. Cereb. Blood Flow Metab. (1982) [Pubmed]
  17. Inhibition of atrial natriuretic peptide-induced cGMP accumulation by purinergic agonists in FRTL-5 thyroid cells. Involvement of both pertussis toxin-sensitive and insensitive mechanisms. Okajima, F., Kondo, Y. J. Biol. Chem. (1990) [Pubmed]
  18. Apoptosis-associated gene expression in the corpus luteum of the rat. Guo, K., Wolf, V., Dharmarajan, A.M., Feng, Z., Bielke, W., Saurer, S., Friis, R. Biol. Reprod. (1998) [Pubmed]
  19. Initial cerebral HM-PAO distribution compared to LCBF: use of a model which considers cerebral HM-PAO trapping kinetics. Lear, J.L. J. Cereb. Blood Flow Metab. (1988) [Pubmed]
  20. Ischemic and reperfused myocardium detected with technetium-99m-nitroimidazole. Fukuchi, K., Kusuoka, H., Watanabe, Y., Fujiwara, T., Nishimura, T. J. Nucl. Med. (1996) [Pubmed]
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