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Gene Review

S100B  -  S100 calcium binding protein B

Homo sapiens

Synonyms: NEF, Protein S100-B, S-100 protein beta chain, S-100 protein subunit beta, S100, ...
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Disease relevance of S100B

  • S100B protein is elevated in the brains of patients with early stages of Alzheimer's disease and Down's syndrome [1].
  • S100 calcium-binding proteins such as S100B are elevated in primary malignant melanoma and are used as markers for this and numerous other cancers [2].
  • Collectively, these findings imply that elevated levels of S100B in tumors such as astrocytomas and gliomas could inhibit p53 functions and contribute to cancer progression [3].
  • There was a significant trend for increasing S100B levels from PP to SP to RR multiple sclerosis (P < 0.05) [4].
  • We also provide evidence that, in human astrocytoma cell lines, S100B co-localizes with IQGAP1 at the polarized leading edge and areas of membrane ruffling and that both proteins relocate in a Ca(2+)-dependent manner within newly formed vesicle-like structures [5].
  • Enteric glial-derived S100B is increased in the duodenum of patients with celiac disease and plays a role in nitric oxide production [6].

Psychiatry related information on S100B


High impact information on S100B


Chemical compound and disease context of S100B


Biological context of S100B

  • But, the differences in the way these proteins bind to p53 could result in S100B and S1004 having different effects on p53 function in cell-cycle control [1].
  • The molecular definition of the monosomy 21 in each patient was, respectively, COL6A1-S100B, CD18-S100B, and PFKL-S100B [20].
  • Comparison to databases indicated three segments matching to known chromosome 21 genes: PFKL, COL6A1 and S100B and six segments matching to unmapped anonymous expressed sequence tags (ESTs) [21].
  • NMR spectroscopy revealed residues most responsive to TRTK-12 binding that could be mapped to the surface of the three-dimensional structure of calcium-saturated S100B, revealing a common region indicative of a binding site [22].
  • Expression of S100B protein in E. coli results in little change in FtsZ protein levels, causes a filamenting bacterial phenotype characteristic of FtsZ inhibition, and leads to missed rounds of cell division [23].

Anatomical context of S100B

  • Cell-based and clinical studies have implicated S100B in the initiation and maintenance of a pathological, glial-mediated proinflammatory state in the central nervous system [24].
  • In glial cells, a relationship exists between cytoplasmic S100B accumulation and cell morphological changes [5].
  • The synthetic peptide TRTK-12 (TRTKIDWNKILS), derived from random bacteriophage library screening, bears sequence similarity to several intermediate filament proteins and has the highest calcium-dependent affinity of any target molecule for S100B to date (K(d) <1 microm) [25].
  • This signaling was inhibited in cells pretreated with soluble RAGE, and S100B was shown to bind to chondrocyte RAGE [26].
  • Our results may explain the rescue of nuclear wild type p53 activities by S100B in fibroblast cell lines expressing the temperature-sensitive p53val135 mutant at the nonpermissive temperature [27].

Associations of S100B with chemical compounds

  • We have identified the IQGAP1 protein as the major cytoplasmic S100B target protein in different rat and human glial cell lines in the presence of Zn(2+) and Ca(2+) [5].
  • The Zn(2+)- and Ca(2+)-binding S100B protein is implicated in multiple intracellular and extracellular regulatory events [5].
  • A pull-down assay using biotin-labeled S100B was used to demonstrate binding to RAGE [26].
  • Here, we probed the putative causal relationship between enhanced astrocytic activation and exacerbation of brain damage in 4/4-KI mice using arundic acid (ONO-2506, Ono Pharmaceutical Co. Ltd), which is known to oppose astrocytic activation through its inhibitory action on S100B synthesis [28].
  • These contributions were quantified using C-terminal mutant S100B proteins lacking the C-terminal seven (S100B85stop) or nine (S100B83stop) residues or containing alanine substitutions at Phe87 (F87A), Phe88 (F88A), or both (F8788A) [29].

Physical interactions of S100B

  • AHNAK binds to S100B-Sepharose beads and is also recovered in anti-S100B immunoprecipitates in a strict Ca(2+)- and Zn(2+)-dependent manner [15].
  • S100A6 and S100A11 are specific targets of the calcium- and zinc-binding S100B protein in vivo [30].
  • Furthermore, p53 binds regions of the S100B promoter, one of which matches the 20-nucleotide p53-binding consensus DNA sequence perfectly [2].
  • S100B is an EF-hand containing calcium-binding protein of the S100 protein family that exerts its biological effect by binding and affecting various target proteins [31].
  • The crystal structure of human EF-hand calcium-binding protein S100A12 in its calcium-bound form has been determined to 1.95 A resolution by molecular replacement using the structure of the S100B protein [32].
  • More importantly, we showed that S100B and S100A6 modulate cell survival in a RAGE-dependent manner; S100B specifically interacted with the RAGE V and C(1) domains and S100A6 specifically interacted with the C(1) and C(2) RAGE domains [33].

Co-localisations of S100B

  • In the peripheral sciatic nerve, nectin-3 immunoreactivity was observed both in controls and following injury and nectin-3 colocalized with both neurofilament and the Schwann cell marker S100 [34].

Regulatory relationships of S100B


Other interactions of S100B

  • Very significant modifications occurred in the level of S100A1 protein expression (and, to a lesser extent, in their of the S100A4 and S100B proteins) in relation to the increasing levels of malignancy [38].
  • There was a correlation between GFAP levels and ambulation in SP multiple sclerosis (r = 0.57, P < 0.01), and between S100B level and the 9HPT in PP multiple sclerosis patients (r = -0.85, P < 0.01) [4].
  • In this report, we show that the S100B protein decreases p53 DNA binding and transcriptional activity [3].
  • They also reveal an additional cellular function for IQGAP1 associated with Zn(2+)/Ca(2+)-dependent relocation of S100B [5].
  • These results suggest that the effects of S100A1 and S100B are not nonspecific effects of low molecular weight, acidic proteins [37].

Analytical, diagnostic and therapeutic context of S100B


  1. Proteins of the S100 family regulate the oligomerization of p53 tumor suppressor. Fernandez-Fernandez, M.R., Veprintsev, D.B., Fersht, A.R. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  2. Inhibiting S100B restores p53 levels in primary malignant melanoma cancer cells. Lin, J., Yang, Q., Yan, Z., Markowitz, J., Wilder, P.T., Carrier, F., Weber, D.J. J. Biol. Chem. (2004) [Pubmed]
  3. Inhibition of p53 transcriptional activity by the S100B calcium-binding protein. Lin, J., Blake, M., Tang, C., Zimmer, D., Rustandi, R.R., Weber, D.J., Carrier, F. J. Biol. Chem. (2001) [Pubmed]
  4. Markers for different glial cell responses in multiple sclerosis: clinical and pathological correlations. Petzold, A., Eikelenboom, M.J., Gveric, D., Keir, G., Chapman, M., Lazeron, R.H., Cuzner, M.L., Polman, C.H., Uitdehaag, B.M., Thompson, E.J., Giovannoni, G. Brain (2002) [Pubmed]
  5. The zinc- and calcium-binding S100B interacts and co-localizes with IQGAP1 during dynamic rearrangement of cell membranes. Mbele, G.O., Deloulme, J.C., Gentil, B.J., Delphin, C., Ferro, M., Garin, J., Takahashi, M., Baudier, J. J. Biol. Chem. (2002) [Pubmed]
  6. Enteric glial-derived S100B protein stimulates nitric oxide production in celiac disease. Esposito, G., Cirillo, C., Sarnelli, G., De Filippis, D., D'Armiento, F.P., Rocco, A., Nardone, G., Petruzzelli, R., Grosso, M., Izzo, P., Iuvone, T., Cuomo, R. Gastroenterology (2007) [Pubmed]
  7. S100B serum levels and long-term improvement of negative symptoms in patients with schizophrenia. Rothermundt, M., Ponath, G., Glaser, T., Hetzel, G., Arolt, V. Neuropsychopharmacology (2004) [Pubmed]
  8. Developmental changes in S100B content in brain tissue, cerebrospinal fluid, and astrocyte cultures of rats. Tramontina, F., Conte, S., Gonçalves, D., Gottfried, C., Portela, L.V., Vinade, L., Salbego, C., Gonçalves, C.A. Cell. Mol. Neurobiol. (2002) [Pubmed]
  9. Cerebrospinal fluid S100B is elevated in the earlier stages of Alzheimer's disease. Peskind, E.R., Griffin, W.S., Akama, K.T., Raskind, M.A., Van Eldik, L.J. Neurochem. Int. (2001) [Pubmed]
  10. Serum S100B is increased during early treatment with antipsychotics and in deficit schizophrenia. Schroeter, M.L., Abdul-Khaliq, H., Frühauf, S., Höhne, R., Schick, G., Diefenbacher, A., Blasig, I.E. Schizophr. Res. (2003) [Pubmed]
  11. S100B is increased in mood disorders and may be reduced by antidepressive treatment. Schroeter, M.L., Abdul-Khaliq, H., Diefenbacher, A., Blasig, I.E. Neuroreport (2002) [Pubmed]
  12. Gene encoding the beta subunit of S100 protein is on chromosome 21: implications for Down syndrome. Allore, R., O'Hanlon, D., Price, R., Neilson, K., Willard, H.F., Cox, D.R., Marks, A., Dunn, R.J. Science (1988) [Pubmed]
  13. Severe immunodeficiency associated with a human immunodeficiency virus 1 NEF/3'-long terminal repeat transgene. Lindemann, D., Wilhelm, R., Renard, P., Althage, A., Zinkernagel, R., Mous, J. J. Exp. Med. (1994) [Pubmed]
  14. Carboxyl-terminal and central regions of human immunodeficiency virus-1 NEF recognized by cytotoxic T lymphocytes from lymphoid organs. An in vitro limiting dilution analysis. Hadida, F., Parrot, A., Kieny, M.P., Sadat-Sowti, B., Mayaud, C., Debre, P., Autran, B. J. Clin. Invest. (1992) [Pubmed]
  15. The giant protein AHNAK is a specific target for the calcium- and zinc-binding S100B protein: potential implications for Ca2+ homeostasis regulation by S100B. Gentil, B.J., Delphin, C., Mbele, G.O., Deloulme, J.C., Ferro, M., Garin, J., Baudier, J. J. Biol. Chem. (2001) [Pubmed]
  16. S100A6 preferentially labels type C nevus cells and nevic corpuscles: additional support for Schwannian differentiation of intradermal nevi. Fullen, D.R., Reed, J.A., Finnerty, B., McNutt, N.S. J. Cutan. Pathol. (2001) [Pubmed]
  17. Evidence of a dominant transcriptional pathway which regulates an undifferentiated and complete metastatic phenotype. Barsky, S.H., Sternlicht, M.D., Safarians, S., Nguyen, M., Chin, K., Stewart, S.D., Hiti, A.L., Gray, J.W. Oncogene (1997) [Pubmed]
  18. Amyotrophic lateral sclerosis: disease stage related changes of tau protein and S100 beta in cerebrospinal fluid and creatine kinase in serum. Süssmuth, S.D., Tumani, H., Ecker, D., Ludolph, A.C. Neurosci. Lett. (2003) [Pubmed]
  19. Activation of RAGE induces elevated O2- generation by mononuclear phagocytes in diabetes. Ding, Y., Kantarci, A., Hasturk, H., Trackman, P.C., Malabanan, A., Van Dyke, T.E. J. Leukoc. Biol. (2007) [Pubmed]
  20. No significant effect of monosomy for distal 21q22.3 on the Down syndrome phenotype in "mirror" duplications of chromosome 21. Pangalos, C., Théophile, D., Sinet, P.M., Marks, A., Stamboulieh-Abazis, D., Chettouh, Z., Prieur, M., Verellen, C., Rethoré, M.O., Lejeune, J. Am. J. Hum. Genet. (1992) [Pubmed]
  21. Model for a transcript map of human chromosome 21: isolation of new coding sequences from exon and enriched cDNA libraries. Yaspo, M.L., Gellen, L., Mott, R., Korn, B., Nizetic, D., Poustka, A.M., Lehrach, H. Hum. Mol. Genet. (1995) [Pubmed]
  22. Specificity and Zn2+ enhancement of the S100B binding epitope TRTK-12. Barber, K.R., McClintock, K.A., Jamieson, G.A., Dimlich, R.V., Shaw, G.S. J. Biol. Chem. (1999) [Pubmed]
  23. Human S100B protein interacts with the Escherichia coli division protein FtsZ in a calcium-sensitive manner. Ferguson, P.L., Shaw, G.S. J. Biol. Chem. (2004) [Pubmed]
  24. Increased susceptibility of S100B transgenic mice to perinatal hypoxia-ischemia. Wainwright, M.S., Craft, J.M., Griffin, W.S., Marks, A., Pineda, J., Padgett, K.R., Van Eldik, L.J. Ann. Neurol. (2004) [Pubmed]
  25. A novel S100 target conformation is revealed by the solution structure of the Ca2+-S100B-TRTK-12 complex. McClintock, K.A., Shaw, G.S. J. Biol. Chem. (2003) [Pubmed]
  26. Articular chondrocytes express the receptor for advanced glycation end products: Potential role in osteoarthritis. Loeser, R.F., Yammani, R.R., Carlson, C.S., Chen, H., Cole, A., Im, H.J., Bursch, L.S., Yan, S.D. Arthritis Rheum. (2005) [Pubmed]
  27. Calcium-dependent interaction of S100B with the C-terminal domain of the tumor suppressor p53. Delphin, C., Ronjat, M., Deloulme, J.C., Garin, G., Debussche, L., Higashimoto, Y., Sakaguchi, K., Baudier, J. J. Biol. Chem. (1999) [Pubmed]
  28. Modulation of astrocytic activation by arundic acid (ONO-2506) mitigates detrimental effects of the apolipoprotein E4 isoform after permanent focal ischemia in apolipoprotein E knock-in mice. Mori, T., Town, T., Tan, J., Tateishi, N., Asano, T. J. Cereb. Blood Flow Metab. (2005) [Pubmed]
  29. The C-terminus and linker region of S100B exert dual control on protein-protein interactions with TRTK-12. McClintock, K.A., Van Eldik, L.J., Shaw, G.S. Biochemistry (2002) [Pubmed]
  30. S100A6 and S100A11 are specific targets of the calcium- and zinc-binding S100B protein in vivo. Deloulme, J.C., Assard, N., Mbele, G.O., Mangin, C., Kuwano, R., Baudier, J. J. Biol. Chem. (2000) [Pubmed]
  31. Recognition of the tumor suppressor protein p53 and other protein targets by the calcium-binding protein S100B. Wilder, P.T., Lin, J., Bair, C.L., Charpentier, T.H., Yang, D., Liriano, M., Varney, K.M., Lee, A., Oppenheim, A.B., Adhya, S., Carrier, F., Weber, D.J. Biochim. Biophys. Acta (2006) [Pubmed]
  32. The three-dimensional structure of human S100A12. Moroz, O.V., Antson, A.A., Murshudov, G.N., Maitland, N.J., Dodson, G.G., Wilson, K.S., Skibshøj, I., Lukanidin, E.M., Bronstein, I.B. Acta Crystallogr. D Biol. Crystallogr. (2001) [Pubmed]
  33. S100B and S100A6 differentially modulate cell survival by interacting with distinct RAGE (receptor for advanced glycation end products) immunoglobulin domains. Leclerc, E., Fritz, G., Weibel, M., Heizmann, C.W., Galichet, A. J. Biol. Chem. (2007) [Pubmed]
  34. Expression of nectin-1, nectin-3, N-cadherin, and NCAM in spinal motoneurons after sciatic nerve transection. Zelano, J., Wallquist, W., Hailer, N.P., Cullheim, S. Exp. Neurol. (2006) [Pubmed]
  35. S100b counteracts effects of the neurotoxicant trimethyltin on astrocytes and microglia. Reali, C., Scintu, F., Pillai, R., Donato, R., Michetti, F., Sogos, V. J. Neurosci. Res. (2005) [Pubmed]
  36. Nomen est Omen: do antidepressants increase p11 or S100A10? Manev, H., Manev, R. Journal of biomedical discovery and collaboration [electronic resource]. (2006) [Pubmed]
  37. Identification of an S100A1/S100B target protein: phosphoglucomutase. Landar, A., Caddell, G., Chessher, J., Zimmer, D.B. Cell Calcium (1996) [Pubmed]
  38. Supratentorial pilocytic astrocytomas, astrocytomas, anaplastic astrocytomas and glioblastomas are characterized by a differential expression of S100 proteins. Camby, I., Nagy, N., Lopes, M.B., Schäfer, B.W., Maurage, C.A., Ruchoux, M.M., Murmann, P., Pochet, R., Heizmann, C.W., Brotchi, J., Salmon, I., Kiss, R., Decaestecker, C. Brain Pathol. (1999) [Pubmed]
  39. Demonstration of heterodimer formation between S100B and S100A6 in the yeast two-hybrid system and human melanoma. Yang, Q., O'Hanlon, D., Heizmann, C.W., Marks, A. Exp. Cell Res. (1999) [Pubmed]
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