p(HGNC:AGER)

Entity

Name

AGER

Namespace

hgnc

Namespace Version

20180906

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Interestingly, resver- atrol downregulated RAGE as well as MMP9 — an effect that is related to decreased hippocampal load of Aβ42 (REF.297) . PubMed:30116051

In AD, these factors are impaired in a number of ways. First, expression of the blood efflux transporters LRP1123 and ABCB1147 is decreased, whereas expression of the blood influx transporter RAGE is upregulated. PubMed:26195256

1,25(OH)2D3, the active form of vitamin D, plays a key role in enhancing transport of Aβ1–40 from the brain to the blood by reducing RAGE levels at the BBB, and also in contributing to periphery clearance by increasing levels of LRP1 both in vivo and in vitro (Guo et al. 2016b) PubMed:29626319

Utilizing Western blot, electrophoretic mobility shift assay, supershift and reverse transcriptase-polymerase chain reaction techniques, it has been demonstrated that micromolar S100B concentrations stimulate c-Jun N-terminal kinase (JNK) phosphorylation through the receptor for advanced glycation ending products, and subsequently activate nuclear AP-1/cJun transcription, in cultured human neural stem cells. In addition, as revealed by Western blot, small interfering RNA and immunofluorescence analysis, S100B-induced JNK activation increased expression of Dickopff-1 that, in turn, promoted glycogen synthase kinase 3β phosphorylation and β-catenin degradation, causing canonical Wnt pathway disruption and tau protein hyperphosphorylation. These findings propose a previously unrecognized link between S100B and tau hyperphosphorylation, suggesting S100B can contribute to NFT formation in AD and in all other conditions in which neuroinflammation may have a crucial role. PubMed:18494933

Utilizing Western blot, electrophoretic mobility shift assay, supershift and reverse transcriptase-polymerase chain reaction techniques, it has been demonstrated that micromolar S100B concentrations stimulate c-Jun N-terminal kinase (JNK) phosphorylation through the receptor for advanced glycation ending products, and subsequently activate nuclear AP-1/cJun transcription, in cultured human neural stem cells. In addition, as revealed by Western blot, small interfering RNA and immunofluorescence analysis, S100B-induced JNK activation increased expression of Dickopff-1 that, in turn, promoted glycogen synthase kinase 3β phosphorylation and β-catenin degradation, causing canonical Wnt pathway disruption and tau protein hyperphosphorylation. These findings propose a previously unrecognized link between S100B and tau hyperphosphorylation, suggesting S100B can contribute to NFT formation in AD and in all other conditions in which neuroinflammation may have a crucial role. PubMed:18494933

Recently, Li et al. (2012b) have demonstrated in their study that AGEs can induce tau hyperphosphorylation through receptor for advanced glycation end product (RAGE)-mediated glycogen synthase kinase 3 (GSK-3) activation and targeting RAGE/GSK-3 pathway can improve AD-like changes. PubMed:24183963

The levels of sRAGE consistently decreased with age (R = −0.264, p = <0.001) and with the indices of obesity, such as BMI. However, of special interest was the highly significant and previ-ously not reported independent correlation with fat free mass (p < 0.001). PubMed:25681682

Here, we found that MG could induce tau hyperphosphorylation at multiple AD-related sites in neuroblastoma 2a cells under maintaining normal cell viability. MG treatment increased the level of advanced glycation end products (AGEs) and the receptor of AGEs (RAGE). PubMed:22798221

The levels of sRAGE consistently decreased with age (R = −0.264, p = <0.001) and with the indices of obesity, such as BMI. However, of special interest was the highly significant and previ-ously not reported independent correlation with fat free mass (p < 0.001). PubMed:25681682

The levels of sRAGE consistently decreased with age (R = −0.264, p = <0.001) and with the indices of obesity, such as BMI. However, of special interest was the highly significant and previ-ously not reported independent correlation with fat free mass (p < 0.001). PubMed:25681682

Collectively, these studies demonstrate that the soluble, astroglial-derived S100B protein interacts with RAGE leading to the JNK phosphorylation and the pJNK-dependent up-regulation of c-Jun, a component of the AP-1 complex. PubMed:18494933

Free Aβ can be transported from the circulation into the interstitium via RAGE (advanced glycosylation end product-specific receptor). PubMed:26195256

In addition, the luminal residing receptor for advanced glycation end products (RAGE) is an Aβ influx transporter (Deane et al. 2003) PubMed:29626319

Utilizing Western blot, electrophoretic mobility shift assay, supershift and reverse transcriptase-polymerase chain reaction techniques, it has been demonstrated that micromolar S100B concentrations stimulate c-Jun N-terminal kinase (JNK) phosphorylation through the receptor for advanced glycation ending products, and subsequently activate nuclear AP-1/cJun transcription, in cultured human neural stem cells. In addition, as revealed by Western blot, small interfering RNA and immunofluorescence analysis, S100B-induced JNK activation increased expression of Dickopff-1 that, in turn, promoted glycogen synthase kinase 3β phosphorylation and β-catenin degradation, causing canonical Wnt pathway disruption and tau protein hyperphosphorylation. These findings propose a previously unrecognized link between S100B and tau hyperphosphorylation, suggesting S100B can contribute to NFT formation in AD and in all other conditions in which neuroinflammation may have a crucial role. PubMed:18494933

Collectively, these studies demonstrate that the soluble, astroglial-derived S100B protein interacts with RAGE leading to the JNK phosphorylation and the pJNK-dependent up-regulation of c-Jun, a component of the AP-1 complex. PubMed:18494933

The levels of sRAGE consistently decreased with age (R = −0.264, p = <0.001) and with the indices of obesity, such as BMI. However, of special interest was the highly significant and previ-ously not reported independent correlation with fat free mass (p < 0.001). PubMed:25681682

The levels of sRAGE consistently decreased with age (R = −0.264, p = <0.001) and with the indices of obesity, such as BMI. However, of special interest was the highly significant and previ-ously not reported independent correlation with fat free mass (p < 0.001). PubMed:25681682

Recently, Li et al. (2012b) have demonstrated in their study that AGEs can induce tau hyperphosphorylation through receptor for advanced glycation end product (RAGE)-mediated glycogen synthase kinase 3 (GSK-3) activation and targeting RAGE/GSK-3 pathway can improve AD-like changes. PubMed:24183963

Then the stimulation of RAGE is able to activate the mitogen-activated protein kinase signaling cascades which converge in IκB kinase complex to phosphorylate IκB, thereby release and activate NF-κB, thus trigger NF-κB dependent gene transcription including IL-1β and TNF-α, which in turn induce the translocation of NF-κB to the nucleus [50]. PubMed:27288790