scholarly article | Q13442814 |
P50 | author | Bernhard Landwehrmeyer | Q42047023 |
Albert C. Ludolph | Q67390363 | ||
P2093 | author name string | S Stamm | |
T Meyer | |||
B Zhu | |||
C Münch | |||
B Schwalenstöcker | |||
M Ebstein | |||
U Seefried | |||
P2860 | cites work | Excitatory amino acid transporter 5, a retinal glutamate transporter coupled to a chloride conductance | Q24313586 |
An excitatory amino-acid transporter with properties of a ligand-gated chloride channel | Q24323343 | ||
Inhibition of translation of transforming growth factor-beta 3 mRNA by its 5' untranslated region | Q24597391 | ||
Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis | Q28131805 | ||
Differential RNA cleavage and polyadenylation of the glutamate transporter EAAT2 in the human brain | Q28141608 | ||
Glutamate transporter EAAT2 splice variants occur not only in ALS, but also in AD and controls | Q28143392 | ||
Expression of the glial glutamate transporter EAAT2 in the human CNS: an immunohistochemical study | Q28260466 | ||
Aberrant RNA processing in a neurodegenerative disease: the cause for absent EAAT2, a glutamate transporter, in amyotrophic lateral sclerosis | Q28267385 | ||
In vivo half-life of a protein is a function of its amino-terminal residue | Q28287702 | ||
Epilepsy and exacerbation of brain injury in mice lacking the glutamate transporter GLT-1 | Q28592689 | ||
Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation | Q29547561 | ||
Alternative pre-mRNA splicing: the logic of combinatorial control | Q29615087 | ||
A rule for termination-codon position within intron-containing genes: when nonsense affects RNA abundance | Q29615731 | ||
Initiation of translation in prokaryotes and eukaryotes | Q29618237 | ||
Alternative splicing: increasing diversity in the proteomic world | Q29618730 | ||
Nonsense-mediated mRNA decay in health and disease | Q29619553 | ||
Tissue specific variants of glutamate transporter GLT-1. | Q30090179 | ||
Selective loss of glial glutamate transporter GLT‐1 in amyotrophic lateral sclerosis | Q34300016 | ||
The release and uptake of excitatory amino acids | Q37607591 | ||
Reduced postischemic expression of a glial glutamate transporter, GLT1, in the rat hippocampus | Q38300706 | ||
Initiation codons within 5'-leaders of mRNAs as regulators of translation | Q40664332 | ||
The 5' UTR of protein kinase C epsilon confers translational regulation in vitro and in vivo | Q40805866 | ||
Elevated cortical extracellular fluid glutamate in transgenic mice expressing human mutant (G93A) Cu/Zn superoxide dismutase | Q42485699 | ||
Evidence for translational repression of the SOCS-1 major open reading frame by an upstream open reading frame | Q42619358 | ||
Splicing of the glutamate transporter EAAT2: a candidate gene of amyotrophic lateral sclerosis | Q42912839 | ||
Transgenic SOD1 G93A mice develop reduced GLT-1 in spinal cord without alterations in cerebrospinal fluid glutamate levels | Q43809083 | ||
ALS-linked SOD1 mutant G85R mediates damage to astrocytes and promotes rapidly progressive disease with SOD1-containing inclusions. | Q46135324 | ||
5'-heterogeneity of the human excitatory amino acid transporter cDNA EAAT2 (GLT-1). | Q47959438 | ||
Activity-dependent regulation of alternative splicing patterns in the rat brain | Q48248567 | ||
SOD1 mutants linked to amyotrophic lateral sclerosis selectively inactivate a glial glutamate transporter | Q48918632 | ||
P433 | issue | 3 | |
P407 | language of work or name | English | Q1860 |
P921 | main subject | amyotrophic lateral sclerosis | Q206901 |
alternative mRNA splicing, via spliceosome | Q21114084 | ||
P304 | page(s) | 594-603 | |
P577 | publication date | 2002-08-01 | |
P1433 | published in | Journal of Neurochemistry | Q6295643 |
P1476 | title | Alternative splicing of the 5'-sequences of the mouse EAAT2 glutamate transporter and expression in a transgenic model for amyotrophic lateral sclerosis | |
P478 | volume | 82 |
Q40480300 | A survey of splice variants of the human hypoxanthine phosphoribosyl transferase and DNA polymerase beta genes: products of alternative or aberrant splicing? |
Q35154322 | Association of rare variation in the glutamate receptor gene SLC1A2 with susceptibility to bipolar disorder and schizophrenia. |
Q35946030 | Biomarkers of neurodegenerative disorders: how good are they? |
Q46902620 | Chemical hypoxia facilitates alternative splicing of EAAT2 in presymptomatic APP23 transgenic mice |
Q44327960 | Differential regulation of 5' splice variants of the glutamate transporter EAAT2 in an in vivo model of chemical hypoxia induced by 3-nitropropionic acid |
Q51824569 | EAAT2 and the Molecular Signature of Amyotrophic Lateral Sclerosis. |
Q36904469 | EAAT2 regulation and splicing: relevance to psychiatric and neurological disorders |
Q51823995 | Exon array analysis of alternative splicing of genes in SOD1G93A transgenic mice. |
Q34181309 | Exon-skipping splice variants of excitatory amino acid transporter-2 (EAAT2) form heteromeric complexes with full-length EAAT2. |
Q26861666 | Glutamate transporter 1: target for the treatment of alcohol dependence |
Q34924292 | Impairment of neuronal glutamate uptake and modulation of the glutamate transporter GLT-1 induced by retinal ischemia |
Q43577107 | Links between electrophysiological and molecular pathology of amyotrophic lateral sclerosis |
Q39625408 | Mutant SOD1 and mitochondrial damage alter expression and splicing of genes controlling neuritogenesis in models of neurodegeneration. |
Q37495425 | SLC1 glutamate transporters |
Q37168377 | The four major N- and C-terminal splice variants of the excitatory amino acid transporter GLT-1 form cell surface homomeric and heteromeric assemblies. |
Q41693925 | The role of glutamate transporters in the pathophysiology of neuropsychiatric disorders |
Q57372610 | Translational Control of Glial Glutamate Transporter EAAT2 Expression |
Q36052481 | Transporters for L-glutamate: an update on their molecular pharmacology and pathological involvement |
Q45246507 | VEGF C2578A polymorphism does not contribute to amyotrophic lateral sclerosis susceptibility in sporadic Chinese patients |
Search more.