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Gene Review

CALB1  -  calbindin 1, 28kDa

Homo sapiens

Synonyms: CAB27, CALB, Calbindin, Calbindin D28, D-28K, ...
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Disease relevance of CALB1

  • An intracellular target of calbindin was discovered using bacteriophage display [1].
  • Our data show that, although the brain pathology is moderate to severe, there is no prominent decrease of PV, CR and CB positive neurons in the visual cortex of Alzheimer brains, but only selective changes in neuronal perikarya [2].
  • Referring to a suggested neuroprotective role of CB, the results may be of relevance in the context of neuronal transplantation of patients suffering from severe Parkinson's disease [3].
  • In the neonate marmoset, large numbers of putative type I ganglion cells from the apical cochlear turn transiently expressed a light and granular labeling for CB-like immunoreactivity, in addition to the cells we believe to be type II ganglion cells exhibiting a strong and solid CB-like staining [4].
  • Fetal hydrocephalus causes severe alterations of CB- and PV-ir neurons in the subplate and the cortical plate: shrinkage of ir neurons, loss of process labeling and in most severe cases, entire loss of immunolabeling [5].

Psychiatry related information on CALB1

  • In post-mortem brain specimens from patients dying with a clinical diagnosis of Huntington's disease (HD) immunohistochemistry showed a substantial loss from the neostriatum of neurons containing the calcium-binding protein calbindin 28K [6].
  • These deficits in PV and CB are notable in also being observed in bipolar disorder, indicating how the close aetiological relationship of these two psychiatric disorders is reflected in their pathology [7].
  • More significantly, interneurons that contain the calcium-binding proteins parvalbumin and calbindin are particularly resistant to degeneration in Alzheimer's disease [8].
  • Compared with other markers, loss of calbindin and parvalbumin interneurons in the frontal cortex was the most significant correlate to memory deficits, suggesting a role in neurobehavioral alterations of HIV(+) METH users [9].
  • In CJD, pathology was severe in pre-parasubiculum and temporal cortex, and little or absent in CA1-4; PV+ neurons were severely reduced or absent in all cases, whereas Cal+ neurons were largely preserved [10].

High impact information on CALB1

  • Using immunofluorescent labeling for BrdU and for one of the neuronal markers, NeuN, calbindin or neuron specific enolase (NSE), we demonstrate that new neurons, as defined by these markers, are generated from dividing progenitor cells in the dentate gyrus of adult humans [11].
  • Immunohistochemical staining showed that this nucleus is defined by a dense calbindin-positive fibre plexus in the macaque, so we applied the same staining method to sections of human thalamus [12].
  • Calbindin-D28K or a related protein may serve as the mobile calcium buffer, an action similar to its function in transporting Ca2+ across intestinal epithelial cells [13].
  • Thus, calbindin occurs in the primate striate cortex in a pattern almost complementary to that displaying strong cytochrome c-oxidase activity [14].
  • Colocalization of neuropeptides with calbindin D28k and NADPH diaphorase in the enteric nerve plexuses of normal human ileum [15].

Chemical compound and disease context of CALB1

  • We show by gain- and loss-of-function in vitro experiments that FGF-20 promotes survival and stimulates dopamine (DA) release in a calbindin-negative subset of cells that are preferentially lost in Parkinson's disease [16].
  • RESULTS: Losses in n-acetylaspartate and calbindin (indicating neuronal injury and/or death) and decreases in synaptophysin immunoreactivity (indicating synaptodendritic injury) were detected along with increases in GFAP (indicating reactive gliosis) [17].
  • The depletion of CB from the BFCN is likely to deprive these neurons of the capacity to buffer high levels of intracellular Ca(2+) and thus to leave them vulnerable to pathological processes, such as those in neurodegenerative disorders, which can cause increased intracellular Ca(2+), thus leading to their degeneration [18].
  • In the rat brain, two weeks after intrastriatal injection of quinolinic acid (6-20 ng), surviving medium-spiny neurons in the transition zone around the lesion core exhibited a marked increase in calbindin immunoreactivity similar to that seen in Huntington's disease spiny neurons [19].
  • To investigate this possibility, we compared the cellular features of calbindin immunoreactivity in grade 1-4 Huntington's disease cases with those seen in rat striatal neurons in vivo and in vitro following treatment with N-methyl-D-aspartate (NMDA) receptor agonist, quinolinic acid [19].

Biological context of CALB1

  • Most importantly, the comparison of CR and Calb domain organizations questions the value of homologous modeling of EF-hand proteins, and perhaps of other protein families [20].
  • Peak cell densities occurred in layer 2/upper layer 3 for CR+ neurons and in upper to midlayer 3 for CB+ cells [21].
  • The sequential arrival of various afferent fiber systems in the two compartments of the striatum (patch and matrix compartment) is reflected by changing patterns of diffuse CB immunolabeling: During the second half of gestation, the patches are labeled and postnatally a changeover to matrix labeling is seen [5].
  • These calbindin neurons, and the straital compartment in which they are sited, are particularly damaged in HD, suggesting that a failure of calcium buffering or homeostasis may contribute to cell death in HD [6].
  • Human calbindin D(28k) is a Ca(2+) binding protein that has been implicated in the protection of cells against apoptosis [22].

Anatomical context of CALB1

  • Cell bodies of interneurons immunoreactive for CB or PV were innervated only occasionally by CR multiterminal endings, whereas certain GABA neurons were surrounded by them [23].
  • The patterns of staining for CalB, CalR, and GABA in the human cortex were similar to those found in monkey neocortex [24].
  • Quantitative distribution of parvalbumin, calretinin, and calbindin D-28k immunoreactive neurons in the visual cortex of normal and Alzheimer cases [2].
  • To verify the possible correspondence of the CB-negative territory with the cerebellar-recipient sector of the motor thalamus, we compared the distribution of cerebello-thalamic projections with the distribution of CBir in two monkeys [25].
  • The substantia nigra is characterized by complementary patterns of high neuropil CB- and SMI-32-ir in pars reticulata (SNr) and high CR-ir in pars compacta (SNc) and in the ventral tegmental area (VTA) [26].

Associations of CALB1 with chemical compounds


Physical interactions of CALB1


Co-localisations of CALB1


Regulatory relationships of CALB1


Other interactions of CALB1

  • Fluorescence spectroscopy showed that isolated calbindin and IMPase interact with an apparent equilibrium dissociation constant, K(D), of 0.9 microm [1].
  • This suggests a common duplication o the calbindin/calretinin and the carbonic anhydrase ancestral genes [37].
  • Neuropil labeling with parvalbumin and calbindin was most dense in layer III of the anterior cingulate cortex [38].
  • In contrast, CB immunoreactivity is prevalent in medial thalamic nuclei (intralaminar and midline), the posterior complex, ventral posterior inferior nucleus, the ventral lateral anterior nucleus, ventral anterior, and ventral medial nuclei [39].
  • A transient supramamillary nucleus was apparent at 14 w.g. but not after 16 w.g. As the ventromedial nucleus differentiated at 13-16 w.g., three principal parts, the ventrolateral part, the dorsomedial part, and the shell, were revealed by distribution of calbindin, calretinin, and GAP43 immunoreactivity [40].

Analytical, diagnostic and therapeutic context of CALB1


  1. Myo-inositol monophosphatase is an activated target of calbindin D28k. Berggard, T., Szczepankiewicz, O., Thulin, E., Linse, S. J. Biol. Chem. (2002) [Pubmed]
  2. Quantitative distribution of parvalbumin, calretinin, and calbindin D-28k immunoreactive neurons in the visual cortex of normal and Alzheimer cases. Leuba, G., Kraftsik, R., Saini, K. Exp. Neurol. (1998) [Pubmed]
  3. GDNF increases the density of cells containing calbindin but not of cells containing calretinin in cultured rat and human fetal nigral tissue. Meyer, M., Zimmer, J., Seiler, R.W., Widmer, H.R. Cell transplantation. (1999) [Pubmed]
  4. Calcium-binding proteins in the spiral ganglion of the monkey, Callithrix jacchus. Spatz, W.B., Löhle, E. Hear. Res. (1995) [Pubmed]
  5. Calcium-binding proteins in the human developing brain. Ulfig, N. Advances in anatomy, embryology, and cell biology. (2002) [Pubmed]
  6. Loss of matrix calcium-binding protein-containing neurons in Huntington's disease. Seto-Ohshima, A., Emson, P.C., Lawson, E., Mountjoy, C.Q., Carrasco, L.H. Lancet (1988) [Pubmed]
  7. Calcium binding protein markers of GABA deficits in schizophrenia--postmortem studies and animal models. Reynolds, G.P., Abdul-Monim, Z., Neill, J.C., Zhang, Z.J. Neurotoxicity research. (2004) [Pubmed]
  8. Calretinin-immunoreactive neocortical interneurons are unaffected in Alzheimer's disease. Hof, P.R., Nimchinsky, E.A., Celio, M.R., Bouras, C., Morrison, J.H. Neurosci. Lett. (1993) [Pubmed]
  9. Cognitive deficits and degeneration of interneurons in HIV+ methamphetamine users. Chana, G., Everall, I.P., Crews, L., Langford, D., Adame, A., Grant, I., Cherner, M., Lazzaretto, D., Heaton, R., Ellis, R., Masliah, E. Neurology (2006) [Pubmed]
  10. Distribution of parvalbumin-immunoreactive neurons in brain correlates with hippocampal and temporal cortical pathology in Creutzfeldt-Jakob disease. Guentchev, M., Hainfellner, J.A., Trabattoni, G.R., Budka, H. J. Neuropathol. Exp. Neurol. (1997) [Pubmed]
  11. Neurogenesis in the adult human hippocampus. Eriksson, P.S., Perfilieva, E., Björk-Eriksson, T., Alborn, A.M., Nordborg, C., Peterson, D.A., Gage, F.H. Nat. Med. (1998) [Pubmed]
  12. A thalamic nucleus specific for pain and temperature sensation. Craig, A.D., Bushnell, M.C., Zhang, E.T., Blomqvist, A. Nature (1994) [Pubmed]
  13. Spatial calcium buffering in saccular hair cells. Roberts, W.M. Nature (1993) [Pubmed]
  14. Calbindin immunoreactivity alternates with cytochrome c-oxidase-rich zones in some layers of the primate visual cortex. Celio, M.R., Schärer, L., Morrison, J.H., Norman, A.W., Bloom, F.E. Nature (1986) [Pubmed]
  15. Colocalization of neuropeptides with calbindin D28k and NADPH diaphorase in the enteric nerve plexuses of normal human ileum. Dhatt, N., Buchan, A.M. Gastroenterology (1994) [Pubmed]
  16. A specific survival response in dopamine neurons at most risk in Parkinson's disease. Murase, S., McKay, R.D. J. Neurosci. (2006) [Pubmed]
  17. Early brain injury in the SIV-macaque model of AIDS. González, R.G., Cheng, L.L., Westmoreland, S.V., Sakaie, K.E., Becerra, L.R., Lee, P.L., Masliah, E., Lackner, A.A. AIDS (2000) [Pubmed]
  18. Loss of calbindin-D28k from aging human cholinergic basal forebrain: relation to neuronal loss. Geula, C., Bu, J., Nagykery, N., Scinto, L.F., Chan, J., Joseph, J., Parker, R., Wu, C.K. J. Comp. Neurol. (2003) [Pubmed]
  19. Quinolinic acid-induced increases in calbindin D28k immunoreactivity in rat striatal neurons in vivo and in vitro mimic the pattern seen in Huntington's disease. Huang, Q., Zhou, D., Sapp, E., Aizawa, H., Ge, P., Bird, E.D., Vonsattel, J.P., DiFiglia, M. Neuroscience (1995) [Pubmed]
  20. Calretinin and calbindin D28k have different domain organizations. Palczewska, M., Groves, P., Batta, G., Heise, B., Kuźnicki, J. Protein Sci. (2003) [Pubmed]
  21. Local circuit neurons in the medial prefrontal cortex (areas 24a,b,c, 25 and 32) in the monkey: I. Cell morphology and morphometrics. Gabbott, P.L., Bacon, S.J. J. Comp. Neurol. (1996) [Pubmed]
  22. Redox sensitive cysteine residues in calbindin D28k are structurally and functionally important. Cedervall, T., Berggård, T., Borek, V., Thulin, E., Linse, S., Akerfeldt, K.S. Biochemistry (2005) [Pubmed]
  23. Synaptic connections of calretinin-immunoreactive neurons in the human neocortex. del Río, M.R., DeFelipe, J. J. Neurosci. (1997) [Pubmed]
  24. Colocalization of calbindin D-28k, calretinin, and GABA immunoreactivities in neurons of the human temporal cortex. del Río, M.R., DeFelipe, J. J. Comp. Neurol. (1996) [Pubmed]
  25. Neurochemical characterization of the cerebellar-recipient motor thalamic territory in the macaque monkey. Calzavara, R., Zappalà, A., Rozzi, S., Matelli, M., Luppino, G. Eur. J. Neurosci. (2005) [Pubmed]
  26. Neurochemical organization of the human basal ganglia: anatomofunctional territories defined by the distributions of calcium-binding proteins and SMI-32. Morel, A., Loup, F., Magnin, M., Jeanmonod, D. J. Comp. Neurol. (2002) [Pubmed]
  27. Chemical anatomy of the human ventral striatum and adjacent basal forebrain structures. Prensa, L., Richard, S., Parent, A. J. Comp. Neurol. (2003) [Pubmed]
  28. Connections of the hippocampal formation in humans: I. The mossy fiber pathway. Lim, C., Blume, H.W., Madsen, J.R., Saper, C.B. J. Comp. Neurol. (1997) [Pubmed]
  29. Calretinin-like immunoreactivity in the optic tectum of the tench (Tinca tinca L.). Arévalo, R., Alonso, J.R., Porteros, A., Briñón, J.G., Crespo, C., Lara, J., Aijón, J. Brain Res. (1995) [Pubmed]
  30. Calbindin D28K interacts with Ran-binding protein M: identification of interacting domains by NMR spectroscopy. Lutz, W., Frank, E.M., Craig, T.A., Thompson, R., Venters, R.A., Kojetin, D., Cavanagh, J., Kumar, R. Biochem. Biophys. Res. Commun. (2003) [Pubmed]
  31. Molecular mechanism of active Ca2+ reabsorption in the distal nephron. Hoenderop, J.G., Nilius, B., Bindels, R.J. Annu. Rev. Physiol. (2002) [Pubmed]
  32. Calbindin D-28k and choline acetyltransferase are expressed by different neuronal populations in pedunculopontine nucleus but not in nucleus basalis in squirrel monkeys. Côté, P.Y., Parent, A. Brain Res. (1992) [Pubmed]
  33. Occurrence of alpha-synuclein pathology in the cerebellum of Guamanian patients with parkinsonism-dementia complex. Sebeo, J., Hof, P.R., Perl, D.P. Acta Neuropathol. (2004) [Pubmed]
  34. Calcium-binding proteins in primate basal ganglia. Parent, A., Fortin, M., Côté, P.Y., Cicchetti, F. Neurosci. Res. (1996) [Pubmed]
  35. Synaptic reorganization of calbindin-positive neurons in the human hippocampal CA1 region in temporal lobe epilepsy. Wittner, L., Eross, L., Szabó, Z., Tóth, S., Czirják, S., Halász, P., Freund, T.F., Maglóczky, Z.S. Neuroscience (2002) [Pubmed]
  36. Expression of calbindin-D28K in motoneuron hybrid cells after retroviral infection with calbindin-D28K cDNA prevents amyotrophic lateral sclerosis IgG-mediated cytotoxicity. Ho, B.K., Alexianu, M.E., Colom, L.V., Mohamed, A.H., Serrano, F., Appel, S.H. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  37. The human calbindin D28k (CALB1) and calretinin (CALB2) genes are located at 8q21.3----q22.1 and 16q22----q23, respectively, suggesting a common duplication with the carbonic anhydrase isozyme loci. Parmentier, M., Passage, E., Vassart, G., Mattei, M.G. Cytogenet. Cell Genet. (1991) [Pubmed]
  38. Neurofilament and calcium-binding proteins in the human cingulate cortex. Nimchinsky, E.A., Vogt, B.A., Morrison, J.H., Hof, P.R. J. Comp. Neurol. (1997) [Pubmed]
  39. Multiarchitectonic and stereotactic atlas of the human thalamus. Morel, A., Magnin, M., Jeanmonod, D. J. Comp. Neurol. (1997) [Pubmed]
  40. Organization of human hypothalamus in fetal development. Koutcherov, Y., Mai, J.K., Ashwell, K.W., Paxinos, G. J. Comp. Neurol. (2002) [Pubmed]
  41. Calretinin and other CaBPs in the nervous system. Rogers, J., Khan, M., Ellis, J. Adv. Exp. Med. Biol. (1990) [Pubmed]
  42. Ca(2+)- and H(+)-dependent conformational changes of calbindin D(28k). Berggård, T., Silow, M., Thulin, E., Linse, S. Biochemistry (2000) [Pubmed]
  43. Interaction of calbindin D28k and inositol monophosphatase in human postmortem cortex: possible implications for bipolar disorder. Shamir, A., Elhadad, N., Belmaker, R.H., Agam, G. Bipolar disorders. (2005) [Pubmed]
  44. Increased neurogenesis in the dentate gyrus after transient global ischemia in gerbils. Liu, J., Solway, K., Messing, R.O., Sharp, F.R. J. Neurosci. (1998) [Pubmed]
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