High impact information on Cit

• Citron is expressed only at low levels in glutamatergic neurons in the hippocampus and is not detectable at synapses onto these neurons [1].
• Neurite outgrowth induced by either agent was blocked by kinase-dead MRCKalpha lacking the p21-binding domain or by a minimal C-terminal regulatory region consisting of the cysteine-rich domain/pleckstrin homology domain plus a region with homology to citron [2].
• Citron-N (citron) binds activated Rho and concentrates at excitatory postsynaptic densities on the smooth dendritic shafts of hippocampal GABAergic neurons [3].
• We first sought to determine whether the synaptic localization machinery is unique to GABAergic interneurons, but in neurons cultured from either cerebral cortex or hippocampus, low levels of citron are found in a small population of glutamatergic neurons concentrated at the tips of dendritic spines in addition to shaft synapses [3].
• Peptides of the general structures H-Xaa-Ala-Ala-Ala-Ala-NH2, H-Ala-Xaa-Ala-Ala-Ala-NH2, and H-Ala-Ala-Xaa-Ala-Ala-NH2 were synthesized, where Xaa is D-Ala, Cit, and all natural amino acids except Cys [4].

Biological context of Cit

• The present results essentially coincided with the amino acid sequence predicted from the nucleotide sequence of the cDNA recently reported by Citron et al [5].
• Citron-kinase, a protein essential to cytokinesis in neuronal progenitors, is deleted in the flathead mutant rat [6].

Anatomical context of Cit

• Desensitization of Ca(2+) flux with different agonists suggests that although tc-LIGRLO-NH(2), Cit, and compound 48/80 have similar mechanisms of action, tc-LIGRLO-NH(2) also activates mast cells by a mechanism distinct from that of 48/80 [7].

Associations of Cit with chemical compounds

• PAR-AP, tc-LIGRLO-NH(2), and Cit increased the free intracellular Ca(2+) concentration, whereas trypsin, tryptase, thrombin, and other PAR-APs did not [7].
• Three synthetic substrates H-Arg-NH-Mec, Bz-Arg-NH-Mec and H-Cit-NH-Mec (Bz, Benzoyl; NH-Mec, 4-methylcoumaryl-7-amide; Cit, citrulline) were used to characterize specificity requirements for the P1-S1 interaction of cathepsin H from rat liver [8].
• The increases in Glu, Asp, Orn and Cit might have resulted from overproduction in the liver, because these contents of the liver increased in stage 2 [9].
• The RD group showed a marked intestinal uptake of Gln and Cit and a net release of Pro, Ala and Gly [10].
• In the standard diet group, plasma Asn+Asp, Thr, Pro, Cit, Trp and Phe levels were higher in rats receiving a glucose solution than in those given saline solution; taurine (on day 20) and Ser (on day 30) showed also higher plasma values [11].

Analytical, diagnostic and therapeutic context of Cit

• Aged (21 months) cognitively-impaired male Sprague-Dawley rats received intraventricular infusion of nerve growth factor (NGF) or cytochrome C (Cit C) for 14 or 28 days using miniosmotic pumps and were evaluated either 1 week or 3 months after treatment [12].

References