NUP98

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NUP98

A gene on chromosome 11p15.5 that encodes a nucleoporin (one of the estimated 50 nucleoporins), which derives from cleavage of a 186-kDa precursor and functions as one of several docking site nucleoporins of transport substrates.

Molecular pathology
NUP98 fuses to several genes after chromosome translocations in acute myeloid leukaemia (AML) and T-cell acute lymphocytic leukaemia (T-ALL), and is one of several genes located in the imprinted gene domain of 11p15.5, a tumour-suppressor gene region. Alterations in 11p15.5 region are associated with the Beckwith-Wiedemann syndrome, Wilms tumour, rhabdomyosarcoma and adrenocortical carcinoma, as well as lung, ovarian and breast cancers.
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For example, it now appears that mutations in ADAR1 that reduce RNA editing are the root cause of Aicardi-Goutieres syndrome, a rare pediatric illness which otherwise resembles viral infection or severe systemic lupus erythematosus (SLE), and mutations in ADAR2 have been linked to a number of neurological disorders.
Ge et al., "Decrease of mRNA editing after spinal cord injury is caused by down-regulation of ADAR2 that is triggered by inflammatory response," Scientific Reports, vol.
Specifically, the research team discovered that proteins ADAR1 and ADAR2, which are involved in the editing of RNA, could potentially be used as a biomarkers to detect disorder leading to gastric cancer.
Our team is the first to conduct a comprehensive analysis demonstrating that changes in RNA sequences, which are caused by the differentially expressed RNA editing enzymes ADAR1 and ADAR2 in gastric tumours, may serve as a novel driving force for gastric cancer, said Asst Prof Chen.
ADAR1 and ADAR2 are two upstream regulators fine-tuning the editing of RNAs and have opposing effects on gastric cancer development.
ADAR2. The upregulation of ADAR2 by chronic treatment with fluoxetine (Table 1) depends on 5-[HT.sub.2B] receptor stimulation, since the 150-200% increase of mRNA and protein expression of ADAR2 was prevented in astrocytes treated with 5-[HT.sub.2B] receptor siRNA [23].
However, the effects of the gene changes of ADAR2, [cPLA.sup.2], and GluK2 are probably not further altered.
Gene Drug FACS, Culture astrocytes astrocytes ADAR2 Fluoxetine Up Up [5-HT.sub.2B] receptor expression Fluoxetine Up Up [5-HT.sub.2B] editing Fluoxetine Up Up [5-HT.sub.2C]receptor expression Fluoxetine Unchanged Unchanged [cPLA.sub.2a] Fluoxetine Up Up [sPLA.sub.2] Fluoxetine Unaltered Unaltered GluK2 expression Fluoxetine Up Up GluK2 editing Fluoxetine Up Up GluK4 expression Fluoxetine Unchanged Unchanged cfos expression Fluoxetine Up Up fosB expression Fluoxetine Up Up [Ca.sub.v ]1.2 Fluoxetine Up Up NBCel Carbamazepine Up Up GluK2 Carbamazepine Down Down [cPLA.sub.2] Carbamazepine Up Up Table 1 shows all experiments in which drug effects were compared in cultured astrocytes and in astrocytes freshly obtained by FACS as described by Lovatt et al.
Within vulnerable neurons, there is selective downregulation of ADAR2 and defective Q/R site editing of the ionotropic glutamatergic AMPA, GluR2 receptor subunit, resulting in the expression of the death-promoting calcium permeable GluR2 isoform and associated impairment in GluR2 mRNA and protein expression, receptor assembly, membrane trafficking, and synaptic targeting.
(21) Se ha observado activacion diferencial de las adenosindeaminasas dependientes de RNA (ADAR1, ADAR2 y RED2) en plasticidad sinaptica e isquemia, (22) especificamente se observa activacion de ADAR2 en isquemia, situacion que explica la regulacion de GluR2 y consecuente vulnerabilidad a esta noxa.