Disease relevance of NUP85

• We report in vivo gene regulation assays where deletion of the N-terminal 75 residues (delta N75) results in loss of transactivation of p53CON and repression of an HPV 6 reporter [1].
• METHODS: Thirteen men cycled for 60 min on four occasions in the same individual hydration status: in normoxia at 55% and 75% of normoxia maximal aerobic power (N55 and N75, respectively), in hypoxia (PB = 594 hPa) at the same absolute workload and at the same relative intensity as N55 (H75 and H55, respectively) [2].
• Response latency is similar in the two groups, but morphology differs, with the N75 component being clearly present in the normal responses, but diminished or undetectable in responses from children with Down's syndrome [3].
• Visual evoked potential: P100 implicit times were delayed in 58 (85.30%) ocular hypertension eyes and 84 (100%) OAG eyes; reduced N75 to P100 amplitudes were observed in 39 (57.35%) ocular hypertension eyes and 73 (86.90%) OAG eyes [4].

Psychiatry related information on NUP85

• The delay in N75 latency was strongly correlated with self-reported years of heroin abuse, but not with years of cocaine, alcohol, or other drug abuse [5].
• Depression of the P60-N75 complex was correlated with the pain-induced loss of proprioception of the foot, making it plausible that this cortical complex reflects neuronal processes leading to perception [6].
• However, children with a positive family history of enuresis showed a shorter latency towards N75 and P100 than children without such a family history [7].

High impact information on NUP85

• Here, we immunodeplete a single subunit, the Nup107-160 complex, using antibodies to Nup85 and Nup133, two of its components [8].
• The results provide strong evidence that the first major component of the VEP elicited by a pattern-reversal stimulus (N75/P85) arises from surface-negative activity in the primary visual cortex (area V1) [9].
• NHE-3, an apically-expressed epithelial isoform which does not possess the N75 N-linked putative glycosylation site and any extracellular loops enriched in serine and threonine residues, does not exhibit any detectable glycosylation [10].
• Collectively, however, the two methadone maintenance groups exhibited significant delays in the N75 and P100 components of the PSVEP relative to the other two groups [5].
• Results indicate that exposure to methylmercury and PCBs resulting from fish and sea mammal consumption were associated with alterations of VEP responses, especially for the latency of the N75 and of the P100 components [11].

Biological context of NUP85

• N75, P100 and N145 waves of the pattern reversal visual evoked potentials were analyzed [12].
• Late cortical components of SEPs and visual evoked potentials with significantly prolonged latencies were recorded in the three younger cases having normal sensory and visual acuity (N35 of SEP, 73.1 +/- 2.1 ms; N75 of VEP, 129.0 +/- 12.7 ms; mean +/- S.D.), while these peaks were absent in the oldest case having the most severe handicap [13].
• The first negative peak in visual evoked response (N75) was bilaterally prolonged, and the median motor (55.9 m/s vs 58.0 m/s) and sensory nerve conduction velocity (55.6 m/s vs 59.0 m/s) were slightly reduced among the highly exposed subjects [14].
• Before and after 12 days of taurine (3 g/day) or placebo supplementation, two identical 2.5-hr VDT work tests were performed while recording the P100, N75 and N145 latencies and P100 amplitude of pattern visual evoked potential (PVEP) and the frequency of critical flicker fusion (CFF) [15].
• Significant differences in P60, N75 and P100 latency and amplitude were found between the two subject groups, especially during the processing of the large visual field [16].

Anatomical context of NUP85

• The earliest response, an N75-P105, focal in the most medial and posterior of the leads implanted in the occipital lobe (lingual g), was probably generated in visual cortical areas 17 and 18 [17].
• During the follow-up period the peak latencies and the P40-N75 IPLs of the tibial nerve SEPs increased and the amplitudes of the tibial nerve SEPs diminished [18].

Associations of NUP85 with chemical compounds

• To examine the functional role of the glycosylation we mutated the four glycosylation sites of the NA1 allele (N39, N75, N163, N170) into glutamine (Q) [19].
• Nevertheless, both the N75 and P100 latencies correlated with the concentration of delta-aminolevulinic acid (delta-ALA) in urine and age [20].
• Significant increases in PREP latencies (N75, P100 and N145) occurred after orally ingesting diphenhydramine [21].
• Visual evoked potentials N75 and P100 latencies correlate with urinary delta-aminolevulinic acid, suggesting gamma-aminobutyric acid involvement in their generation [20].
• Pattern shift visual evoked potential (PSVEP) N75 and P100 latencies were evaluated as an objective, widely available and rapid test of brain dysfunction in a group of 11 patients in the acute phase (first 6 h) of mild-to-moderate carbon monoxide (CO) poisoning [22].

Analytical, diagnostic and therapeutic context of NUP85

• This study showed that the P100 latency was significantly delayed in patients with diabetes compared with the control group (p<0.01), while the N75 to P100 amplitude was similar in both groups [23].

References