Disease relevance of Rpl4

• We also examined the expression of L1, a cell adhesion molecule suspected of involvement in the genesis of hydrocephalus after prenatal ethanol exposure, in 1-day-old rats [1].

Psychiatry related information on Rpl4

• In this study, we sought to investigate whether differences in the steady-state levels of L1 and NCAM expression in specific brain regions could account for individual differences in learning abilities [2].

High impact information on Rpl4

• Induction of L1 mRNA in PC12 cells by NGF is modulated by cell-cell contact and does not require the high-affinity NGF receptor [3].
• The effect of NGF on L1 mRNA was greatest in cells cultured at high density, but its effect on cells cultured at low density was augmented by antibody to L1 (to mimic L1 homophilic binding) [3].
• After 7 d exposure to NGF, but not after exposure to EGF, FGF, TGF beta, or dibutyryl cAMP (dbcAMP), L1 mRNA levels increased fourfold [3].
• The peptides, which include Ser1152, inhibit neurite outgrowth on L1 but not on a control substrate, laminin [4].
• Based on these peptide assays and sequencing of radiolabeled L1 proteolytic fragments, the phosphorylation site was determined to be Ser1152 [4].

Biological context of Rpl4

• From the results, it is suggested that rpL4 would have certain roles in cell proliferation and differentiation during neurogenesis, but have no roles in 5AzC-induced apoptosis in the fetal brain [5].
• Involvement of p90rsk in neurite outgrowth mediated by the cell adhesion molecule L1 [4].
• The relationship of methylation to the evolutionary history and fate of the rat L1 promoter is discussed [6].
• The G + C rich promoter contains enough CpGs to qualify it as a CpG island, but in contrast to other CpG islands, genomic L1 promoters are fully methylated in both somatic cell and sperm DNA as judged by restriction enzyme analysis [6].
• Activation only occurs when the promoter region is oriented to the transferase gene as it is to the L1 protein encoding sequences and is 75% inhibited by methylation of just 5 of the 22 CpGs present in the promoter [6].

Anatomical context of Rpl4

• 5AzC also induces apoptosis in undifferentiated PC12 cells, and ribosomal protein L4 (rpL4) mRNA expression increases prior to apoptosis [5].
• Only few TUNEL-positive cells were observed in VZ, SVZ, cerebral cortex, EGL, and hippocampus during embryonic and early postnatal days, and the regions with TUNEL-positive cells were not identical to rpL4 mRNA distribution [5].
• Next, the changes of rpL4 mRNA expression in the brain of 5AzC-treated rat fetuses were examined by in situ hybridization and RT-PCR [5].
• Here we report that the 600 bp promoter-like region at the left end of a newly isolated and characterized rat L1 DNA element can activate the prokaryotic chloramphenicol acyltransferase gene in a rat cell line [6].
• Many large sensory neurons expressed neither L1 nor CHL1 mRNAs and motor neurons expressed little or no CHL1 mRNA [7].

Associations of Rpl4 with chemical compounds

• Expression of ribosomal protein L4 (rpL4) during neurogenesis and 5-azacytidine (5AzC)-induced apoptotic process in the rat [5].
• Neuronal activity (increased with 25 mM K+, 100 microns N-methyl-D-aspartate, and 100 microns 4-aminopyridine) enhanced L1 transcription and translation [8].
• Age-related increases in cerebral arterial wall thickness and wall:lumen ratio were not affected (L1) or limited slightly (L10) by losartan [9].
• Maximal inhibition of L1 expression was observed at concentrations of 10(-7) M dexamethasone, and the decrease occurred during the second day of treatment [10].
• The effects of dibutyryl cyclic AMP and phorbol ester on the glucocorticoid and NGF regulation of L1 protein were also examined [10].

Analytical, diagnostic and therapeutic context of Rpl4

• With Northern blots we find peak expression of L1 RNA at postnatal day 1 (P1) in the developing rat brain [8].
• Western blot analysis demonstrated that the L1 kinase activity from PC12 cells that phosphorylated this site was co-eluted with the S6 kinase, p90(rsk) [4].
• Neither motor nor sensory neurons showed any obvious upregulation of L1 mRNA after axotomy [7].
• Analysis of the mRNA levels by PCR and northern blots indicated that glucocorticoids reduced the L1 mRNA, whereas NGF increased the level of L1 mRNA [10].
• Immunoelectron microscopy localized L1 to the surface of unmyelinated axons in both normal and deafferented dentate gyrus [11].

References