The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

Links

 

Gene Review

Sptan1  -  spectrin alpha, non-erythrocytic 1

Mus musculus

Synonyms: 2610027H02Rik, Alpha-II spectrin, Fodrin alpha chain, Spectrin alpha chain, non-erythrocytic 1, Spna-2, ...
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of Spna2

  • Previously, we found a cleavage product of 120-kDa alpha-fodrin as an important autoantigen in the pathogenesis of primary Sjögren's syndrome (SS) [1].
  • In brain-derived cells, HIV-1 envelope glycoprotein gp120 initiates a signaling cascade that involves p38 mitogen-activated protein kinase and leads to neuronal cell death [2].
  • They are present in gliomas and may be responsible for the lethality of these incurable brain tumors [3].
  • To address this issue, IgG phage display libraries were generated from the bone marrow of two SS donors and a panel of anti-alpha-fodrin IgGs was isolated by selection on alpha-fodrin immunoblots [4].
  • The lack of MyD88-dependent signals had a dramatic effect on the extent of tissue injury, with significantly larger brain abscesses typified by exaggerated edema and necrosis in MyD88 KO animals [5].
 

Psychiatry related information on Spna2

  • Our theory leads to predictions for sleep time, sleep cycle time, and rapid eye movement time as functions of body and brain mass, and it explains, for example, why mice sleep approximately 14 hours per day relative to the 3.5 hours per day that elephants sleep [6].
  • Additionally, the haplotype A was associated with increased volume of brain white matter that in turn correlated with performance in the vocabulary test [7].
  • Thus, partial reduction (maintaining a level above 50% of normal) of brain nicastrin would likely not be efficacious in reducing functional PS-complexes and gamma-secretase activity as a therapeutic strategy for Alzheimer's disease [8].
  • In conclusion, oxidative damage in nucleic acids is likely to be a major risk factor for Parkinson's disease, indicating that a solid understanding of the defense mechanisms involved will enable us to develop new strategies for protecting the brain against oxidative stress [9].
  • Brain-derived neurotrophic factor (BDNF) has important functions in the development of the nervous system and in brain plasticity-related processes such as memory, learning, and drug addiction [10].
 

High impact information on Spna2

  • Identification of alpha-fodrin as a candidate autoantigen in primary Sjögren's syndrome [11].
  • After beta-actin, the cytosolic brain isoform of creatine kinase was the next most abundant bundle protein; at approximately 0.5 mM, creatine kinase is capable of maintaining high ATP levels despite 1 mM/s ATP consumption by the plasma-membrane Ca(2+)-ATPase [12].
  • Here we demonstrated that multiple isoforms of SH2B1 (alpha, beta, gamma, and/or delta) were expressed in numerous tissues, including the brain, hypothalamus, liver, muscle, adipose tissue, heart, and pancreas [13].
  • We further show that alpha-fodrin, a substrate of the interleukin 1beta-converting enzyme (ICE) and CED-3 family of cysteine proteases, becomes proteolytically cleaved in cells undergoing cell death by increased c-Jun activity [14].
  • This is evidence that prefrontal cortical norepinephrine transmission is necessary for motivational salience attribution to both reward- and aversion-related stimuli through modulation of dopamine in nucleus accumbens, a brain area involved in all motivated behaviors [15].
 

Chemical compound and disease context of Spna2

  • Gender and estrogen manipulation do not affect traumatic brain injury in mice [16].
  • This genus-specific small-subunit (18S) rRNA gene-based PCR can complement conventional (immuno-) histology for the diagnosis of primary amoebic meningoencephalitis in paraffin-embedded brain necropsy specimens that had been fixed in formalin buffered with phosphate-buffered saline [17].
  • We report the novel presence of oxidized phosphatidylcholine [1-palmitoyl-2-(5'-oxo)valeryl-sn-glycero-3-phosphorylcholine (POVPC)], a lipid associated with inflammatory diseases such as atherosclerosis and lung disease, in the brain of MS patients [18].
  • In particular, potential bioenergetic and neural mechanisms for anticonvulsant efficacy of fluoxetine were explored using food intake/body weight monitoring and quantification of brain serotonin transporter protein [19].
  • Whether diabetes mellitus changed the distribution of phenobarbital (60 mg/kg, i.v.) in brain of mice was measured, and whether the changed distribution caused the difference of phenobarbital (80 and 100 mg/kg) -induced loss of the righting reflex in non-diabetic and diabetic mice were also investigated [20].
 

Biological context of Spna2

  • The mouse Il 1rn gene was mapped to the proximal region of chromosome 2 between the centromere and Spna2; the other known members of the mouse IL-1 gene family, Il 1a and Il 1b, both map to the same chromosome, although not in close linkage [21].
  • The estimated map distances and most likely gene order are centromere-Pax-8-2.1 +/- 1.2-us-0.7 +/- 0.7-Spna-2; however, the reverse order cannot be ruled out [22].
  • Cloning and deletion mutagenesis using direct protein-protein interaction on an expression vector. Identification of the calmodulin binding domain of alpha-fodrin [23].
  • Here we demonstrate conditional regulation of gene expression from electroporated plasmids in the postnatal rat retina and the embryonic mouse brain [24].
  • Complete deficiency in nucleotide excision repair therefore renders the brain profoundly sensitive to neurodegeneration in specific cell types of the cerebellum, possibly because of unrepaired endogenous DNA damage that is a substrate for nucleotide but not base excision repair [25].
 

Anatomical context of Spna2

 

Associations of Spna2 with chemical compounds

  • Repeated Methamphetamine Administration Alters Expression of the NMDA Receptor Channel {varepsilon}2 Subunit and Kinesins in the Mouse Brain [30].
  • Ca2+/Calmodulin Kinase Kinase {alpha} Is Dispensable for Brain Development but Is Required for Distinct Memories in Male, though Not in Female, Mice [31].
  • The antioxidant edaravone decreased oxidative stress in damaged brains, more pronounced in the Hq mice, and further reduced brain injury in Hq but not in Wt mice [32].
  • We showed that the PrP in C4/- mice does not functionally rescue the Prnp(-/-) phenotype; furthermore it is unable to undergo beta cleavage, although an increased amount of C1 fragments was found in ischemic brain areas compared with sham controls [33].
  • A Requirement for Microglial TLR4 in Leukocyte Recruitment into Brain in Response to Lipopolysaccharide [34].
 

Regulatory relationships of Spna2

 

Other interactions of Spna2

  • Our data make it unlikely that us is a mutation in either Spna-2 or Pax-8 [22].
  • The brain alpha-spectrin (alpha-fodrin) gene is located on the centromeric end of chromosome 2 and is not closely linked to any previously mapped erythroid or neurological mutation [37].
  • In the view of a role of the retinal Miller glia as a source of neural protection in the retina, the increased astrocytic population in the Bmi1-/- brain led us to investigate the effect of Bmi1 loss in Rd1 mice [38].
  • Caspase-3 is required for alpha-fodrin cleavage but dispensable for cleavage of other death substrates in apoptosis [35].
  • Remarkably, transcriptional expression of alpha-fodrin was retained in the Aire-deficient thymus [39].
 

Analytical, diagnostic and therapeutic context of Spna2

References

  1. Prevention and induction of autoimmune exocrinopathy is dependent on pathogenic autoantigen cleavage in murine Sjögren's syndrome. Saegusa, K., Ishimaru, N., Yanagi, K., Mishima, K., Arakaki, R., Suda, T., Saito, I., Hayashi, Y. J. Immunol. (2002) [Pubmed]
  2. HIV-1 coreceptors CCR5 and CXCR4 both mediate neuronal cell death but CCR5 paradoxically can also contribute to protection. Kaul, M., Ma, Q., Medders, K.E., Desai, M.K., Lipton, S.A. Cell Death Differ. (2007) [Pubmed]
  3. HEDGEHOG-GLI1 Signaling Regulates Human Glioma Growth, Cancer Stem Cell Self-Renewal, and Tumorigenicity. Clement, V., Sanchez, P., de Tribolet, N., Radovanovic, I., Ruiz I Altaba, A. Curr. Biol. (2007) [Pubmed]
  4. Molecular analysis of the human autoantibody response to alpha-fodrin in Sjögren's syndrome reveals novel apoptosis-induced specificity. Maruyama, T., Saito, I., Hayashi, Y., Kompfner, E., Fox, R.I., Burton, D.R., Ditzel, H.J. Am. J. Pathol. (2004) [Pubmed]
  5. MyD88-Dependent Signals Are Essential for the Host Immune Response in Experimental Brain Abscess. Kielian, T., Phulwani, N.K., Esen, N., Syed, M.M., Haney, A.C., McCastlain, K., Johnson, J. J. Immunol. (2007) [Pubmed]
  6. A quantitative, theoretical framework for understanding mammalian sleep. Savage, V.M., West, G.B. Proc. Natl. Acad. Sci. U.S.A. (2007) [Pubmed]
  7. Plexin B3 is genetically associated with verbal performance and white matter volume in human brain. Rujescu, D., Meisenzahl, E.M., Krejcova, S., Giegling, I., Zetzsche, T., Reiser, M., Born, C.M., Möller, H.J., Veske, A., Gal, A., Finckh, U. Mol. Psychiatry (2007) [Pubmed]
  8. Excess of nicastrin in brain results in heterozygosity having no effect on endogenous APP processing and amyloid peptide levels in vivo. Brijbassi, S., Amtul, Z., Newbigging, S., Westaway, D., St George-Hyslop, P., Rozmahel, R.F. Neurobiol. Dis. (2007) [Pubmed]
  9. Oxidative damage in nucleic acids and Parkinson's disease. Nakabeppu, Y., Tsuchimoto, D., Yamaguchi, H., Sakumi, K. J. Neurosci. Res. (2007) [Pubmed]
  10. Mouse and rat BDNF gene structure and expression revisited. Aid, T., Kazantseva, A., Piirsoo, M., Palm, K., Timmusk, T. J. Neurosci. Res. (2007) [Pubmed]
  11. Identification of alpha-fodrin as a candidate autoantigen in primary Sjögren's syndrome. Haneji, N., Nakamura, T., Takio, K., Yanagi, K., Higashiyama, H., Saito, I., Noji, S., Sugino, H., Hayashi, Y. Science (1997) [Pubmed]
  12. Hair Bundles Are Specialized for ATP Delivery via Creatine Kinase. Shin, J.B., Streijger, F., Beynon, A., Peters, T., Gadzala, L., McMillen, D., Bystrom, C., Van der Zee, C.E., Wallimann, T., Gillespie, P.G. Neuron (2007) [Pubmed]
  13. Neuronal SH2B1 is essential for controlling energy and glucose homeostasis. Ren, D., Zhou, Y., Morris, D., Li, M., Li, Z., Rui, L. J. Clin. Invest. (2007) [Pubmed]
  14. Induction of apoptosis by the transcription factor c-Jun. Bossy-Wetzel, E., Bakiri, L., Yaniv, M. EMBO J. (1997) [Pubmed]
  15. Prefrontal/accumbal catecholamine system determines motivational salience attribution to both reward- and aversion-related stimuli. Ventura, R., Morrone, C., Puglisi-Allegra, S. Proc. Natl. Acad. Sci. U.S.A. (2007) [Pubmed]
  16. Gender and estrogen manipulation do not affect traumatic brain injury in mice. Bruce-Keller, A.J., Dimayuga, F.O., Reed, J.L., Wang, C., Angers, R., Wilson, M.E., Dimayuga, V.M., Scheff, S.W. J. Neurotrauma (2007) [Pubmed]
  17. PCR-Based Diagnosis of Naegleria sp. Infection in Formalin-Fixed and Paraffin-Embedded Brain Sections. Schild, M., Gianinazzi, C., Gottstein, B., Müller, N. J. Clin. Microbiol. (2007) [Pubmed]
  18. Oxidized phosphatidylcholine is a marker for neuroinflammation in multiple sclerosis brain. Qin, J., Goswami, R., Balabanov, R., Dawson, G. J. Neurosci. Res. (2007) [Pubmed]
  19. Seizure prophylaxis in an animal model of epilepsy by dietary fluoxetine supplementation. Richman, A., Heinrichs, S.C. Epilepsy Res. (2007) [Pubmed]
  20. Attenuated function and expression of P-glycoprotein at blood-brain barrier and increased brain distribution of phenobarbital in streptozotocin-induced diabetic mice. Liu, H., Zhang, D., Xu, X., Liu, X., Wang, G., Xie, L., Pang, X., Liu, L. Eur. J. Pharmacol. (2007) [Pubmed]
  21. Mouse IL-1 receptor antagonist protein. Molecular characterization, gene mapping, and expression of mRNA in vitro and in vivo. Zahedi, K., Seldin, M.F., Rits, M., Ezekowitz, R.A., Whitehead, A.S. J. Immunol. (1991) [Pubmed]
  22. Urogenital syndrome (us): a developmental mutation on chromosome 2 of the mouse. Lane, P.W., Birkenmeier, C.S. Mamm. Genome (1993) [Pubmed]
  23. Cloning and deletion mutagenesis using direct protein-protein interaction on an expression vector. Identification of the calmodulin binding domain of alpha-fodrin. Sri Widada, J., Asselin, J., Colote, S., Marti, J., Ferraz, C., Travé, G., Haiech, J., Liautard, J.P. J. Mol. Biol. (1989) [Pubmed]
  24. Controlled expression of transgenes introduced by in vivo electroporation. Matsuda, T., Cepko, C.L. Proc. Natl. Acad. Sci. U.S.A. (2007) [Pubmed]
  25. Increased apoptosis, p53 up-regulation, and cerebellar neuronal degeneration in repair-deficient Cockayne syndrome mice. Laposa, R.R., Huang, E.J., Cleaver, J.E. Proc. Natl. Acad. Sci. U.S.A. (2007) [Pubmed]
  26. Na,K-ATPase in skeletal muscle: two populations of beta-spectrin control localization in the sarcolemma but not partitioning between the sarcolemma and the transverse tubules. Williams, M.W., Resneck, W.G., Kaysser, T., Ursitti, J.A., Birkenmeier, C.S., Barker, J.E., Bloch, R.J. J. Cell. Sci. (2001) [Pubmed]
  27. Cytoskeleton and vesicle mobility in astrocytes. Potokar, M., Kreft, M., Li, L., Daniel Andersson, J., Pangrsic, T., Chowdhury, H.H., Pekny, M., Zorec, R. Traffic (2007) [Pubmed]
  28. Not just a plasma membrane protein: in cardiac muscle cells alpha-II spectrin also shows a close association with myofibrils. Bennett, P.M., Baines, A.J., Lecomte, M.C., Maggs, A.M., Pinder, J.C. J. Muscle Res. Cell. Motil. (2004) [Pubmed]
  29. Cysteinyl leukotriene receptor 1 is involved in N-methyl-D-aspartate-mediated neuronal injury in mice. Ding, Q., Wei, E.Q., Zhang, Y.J., Zhang, W.P., Chen, Z. Acta Pharmacol. Sin. (2006) [Pubmed]
  30. Repeated Methamphetamine Administration Alters Expression of the NMDA Receptor Channel {varepsilon}2 Subunit and Kinesins in the Mouse Brain. Yamamoto, H., Imai, K., Kamegaya, E., Takamatsu, Y., Irago, M., Hagino, Y., Kasai, S., Shimada, K., Yamamoto, T., Sora, I., Koga, H., Ikeda, K. Ann. N. Y. Acad. Sci. (2006) [Pubmed]
  31. Ca2+/Calmodulin Kinase Kinase {alpha} Is Dispensable for Brain Development but Is Required for Distinct Memories in Male, though Not in Female, Mice. Mizuno, K., Ris, L., S??nchez-Capelo, A., Godaux, E., Giese, K.P. Mol. Cell. Biol. (2006) [Pubmed]
  32. Apoptosis-inducing factor is a major contributor to neuronal loss induced by neonatal cerebral hypoxia-ischemia. Zhu, C., Wang, X., Huang, Z., Qiu, L., Xu, F., Vahsen, N., Nilsson, M., Eriksson, P.S., Hagberg, H., Culmsee, C., Plesnila, N., Kroemer, G., Blomgren, K. Cell Death Differ. (2007) [Pubmed]
  33. The role of the octarepeat region in neuroprotective function of the cellular prion protein. Mitteregger, G., Vosko, M., Krebs, B., Xiang, W., Kohlmannsperger, V., Nölting, S., Hamann, G.F., Kretzschmar, H.A. Brain Pathol. (2007) [Pubmed]
  34. A Requirement for Microglial TLR4 in Leukocyte Recruitment into Brain in Response to Lipopolysaccharide. Zhou, H., Lapointe, B.M., Clark, S.R., Zbytnuik, L., Kubes, P. J. Immunol. (2006) [Pubmed]
  35. Caspase-3 is required for alpha-fodrin cleavage but dispensable for cleavage of other death substrates in apoptosis. Jänicke, R.U., Ng, P., Sprengart, M.L., Porter, A.G. J. Biol. Chem. (1998) [Pubmed]
  36. Activation of multiple pathways during photoreceptor apoptosis in the rd mouse. Doonan, F., Donovan, M., Cotter, T.G. Invest. Ophthalmol. Vis. Sci. (2005) [Pubmed]
  37. Chromosomal location of three spectrin genes: relationship to the inherited hemolytic anemias of mouse and man. Birkenmeier, C.S., McFarland-Starr, E.C., Barker, J.E. Proc. Natl. Acad. Sci. U.S.A. (1988) [Pubmed]
  38. BMI1 loss delays photoreceptor degeneration in Rd1 mice. Bmi1 loss and neuroprotection in Rd1 mice. Zencak, D., Crippa, S.V., Tekaya, M., Tanger, E., Schorderet, D.E., Munier, F.L., van Lohuizen, M., Arsenijevic, Y. Adv. Exp. Med. Biol. (2006) [Pubmed]
  39. Development of autoimmunity against transcriptionally unrepressed target antigen in the thymus of Aire-deficient mice. Kuroda, N., Mitani, T., Takeda, N., Ishimaru, N., Arakaki, R., Hayashi, Y., Bando, Y., Izumi, K., Takahashi, T., Nomura, T., Sakaguchi, S., Ueno, T., Takahama, Y., Uchida, D., Sun, S., Kajiura, F., Mouri, Y., Han, H., Matsushima, A., Yamada, G., Matsumoto, M. J. Immunol. (2005) [Pubmed]
  40. Autoantigen-specific CD4+CD28low T cell subset prevents autoimmune exocrinopathy in murine Sjögren's syndrome. Saegusa, K., Ishimaru, N., Yanagi, K., Haneji, N., Nishino, M., Azuma, M., Saito, I., Hayashi, Y. J. Immunol. (2000) [Pubmed]
  41. Wavelet-based multi-resolution statistics for optical imaging signals: Application to automated detection of odour activated glomeruli in the mouse olfactory bulb. Bathellier, B., Van De Ville, D., Blu, T., Unser, M., Carleton, A. Neuroimage (2007) [Pubmed]
  42. Severe destructive autoimmune lesions with aging in murine Sjögren's syndrome through Fas-mediated apoptosis. Ishimaru, N., Yoneda, T., Saegusa, K., Yanagi, K., Haneji, N., Moriyama, K., Saito, I., Hayashi, Y. Am. J. Pathol. (2000) [Pubmed]
  43. Development of autoimmune exocrinopathy resembling Sjögren's syndrome in estrogen-deficient mice of healthy background. Ishimaru, N., Arakaki, R., Watanabe, M., Kobayashi, M., Miyazaki, K., Hayashi, Y. Am. J. Pathol. (2003) [Pubmed]
 
WikiGenes - Universities