FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3217569112> ?p ?o ?g. }

• W3217569112 endingPage "12533" @default.
• W3217569112 startingPage "12533" @default.
• W3217569112 abstract "In the present study, we investigated the involvement of the chaperone protein BiP (also known as GRP78 or Hspa5), a master regulator of intracellular proteostasis, in two mouse models of neurodegenerative diseases: amyotrophic lateral sclerosis (ALS) and Parkinson's disease (PD). To this end, we used mice bearing partial genetic deletion of the BiP gene (BiP+/- mice), which, for the ALS model, were crossed with mutant SOD1 (mSOD1) transgenic mice to generate mSOD1/BiP+/- double mutant mice. Our data revealed a more intense neurological decline in the double mutants, reflected in a greater deterioration of the neurological score and rotarod performance, with also a reduced animal survival, compared to mSOD1 transgenic mice. Such worsening was associated with higher microglial (labelled with Iba-1 immunostaining) and, to a lesser extent, astroglial (labelled with GFAP immunostaining) immunoreactivities found in the double mutants, but not with a higher loss of spinal motor neurons (labelled with Nissl staining) in the spinal cord. The morphological analysis of Iba-1 and GFAP-positive cells revealed a higher presence of activated cells, characterized by elevated cell body size and shorter processes, in double mutants compared to mSOD1 mice with normal BiP expression. In the case of the PD model, BiP+/- mice were unilaterally lesioned with the parkinsonian neurotoxin 6-hydroxydopamine (6-OHDA). In this case, however, we did not detect a greater susceptibility to damage in mutant mice, as the motor defects caused by 6-OHDA in the pole test and the cylinder rearing test, as well as the losses in tyrosine hydroxylase-containing neurons and the elevated glial reactivity (labelled with CD68 and GFAP immunostaining) detected in the substantia nigra were of similar magnitude in BiP+/- mice compared with wildtype animals. Therefore, our findings support the view that a dysregulation of the protein BiP may contribute to ALS pathogenesis. As BiP has been recently related to cannabinoid type-1 (CB1) receptor function, our work also opens the door to future studies on a possible link between BiP and the neuroprotective effects of cannabinoids that have been widely reported in this neuropathological context. In support of this possibility, preliminary data indicate that CB1 receptor levels are significantly reduced in mSOD1 mice having partial deletion of BiP gene." @default.
• W3217569112 created "2021-12-06" @default.
• W3217569112 creator A5008498660 @default.
• W3217569112 creator A5017206069 @default.
• W3217569112 creator A5018669039 @default.
• W3217569112 creator A5036189795 @default.
• W3217569112 creator A5043016138 @default.
• W3217569112 creator A5049331909 @default.
• W3217569112 creator A5061436981 @default.
• W3217569112 creator A5075936386 @default.
• W3217569112 creator A5077063484 @default.
• W3217569112 creator A5083930081 @default.
• W3217569112 date "2021-11-20" @default.
• W3217569112 modified "2023-10-05" @default.
• W3217569112 title "BiP Heterozigosity Aggravates Pathological Deterioration in Experimental Amyotrophic Lateral Sclerosis" @default.
• W3217569112 cites W1146102393 @default.
• W3217569112 cites W1536828728 @default.
• W3217569112 cites W1602202713 @default.
• W3217569112 cites W1943627496 @default.
• W3217569112 cites W1967493869 @default.
• W3217569112 cites W1980388563 @default.
• W3217569112 cites W1998934835 @default.
• W3217569112 cites W2005019545 @default.
• W3217569112 cites W2005194978 @default.
• W3217569112 cites W2009980006 @default.
• W3217569112 cites W2041353400 @default.
• W3217569112 cites W2077467150 @default.
• W3217569112 cites W2079856528 @default.
• W3217569112 cites W2106182910 @default.
• W3217569112 cites W2114447482 @default.
• W3217569112 cites W2123184750 @default.
• W3217569112 cites W2149749110 @default.
• W3217569112 cites W2163411496 @default.
• W3217569112 cites W2172278003 @default.
• W3217569112 cites W2562322488 @default.
• W3217569112 cites W2605139437 @default.
• W3217569112 cites W2735187859 @default.
• W3217569112 cites W2747266557 @default.
• W3217569112 cites W2767738407 @default.
• W3217569112 cites W2807482700 @default.
• W3217569112 cites W2851752705 @default.
• W3217569112 cites W2887287732 @default.
• W3217569112 cites W2887594646 @default.
• W3217569112 cites W2906876155 @default.
• W3217569112 cites W2914319179 @default.
• W3217569112 cites W3109820505 @default.
• W3217569112 cites W3187691447 @default.
• W3217569112 doi "https://doi.org/10.3390/ijms222212533" @default.
• W3217569112 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8621319" @default.
• W3217569112 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34830414" @default.
• W3217569112 hasPublicationYear "2021" @default.
• W3217569112 type Work @default.
• W3217569112 sameAs 3217569112 @default.
• W3217569112 citedByCount "5" @default.
• W3217569112 countsByYear W32175691122022 @default.
• W3217569112 countsByYear W32175691122023 @default.
• W3217569112 crossrefType "journal-article" @default.
• W3217569112 hasAuthorship W3217569112A5008498660 @default.
• W3217569112 hasAuthorship W3217569112A5017206069 @default.
• W3217569112 hasAuthorship W3217569112A5018669039 @default.
• W3217569112 hasAuthorship W3217569112A5036189795 @default.
• W3217569112 hasAuthorship W3217569112A5043016138 @default.
• W3217569112 hasAuthorship W3217569112A5049331909 @default.
• W3217569112 hasAuthorship W3217569112A5061436981 @default.
• W3217569112 hasAuthorship W3217569112A5075936386 @default.
• W3217569112 hasAuthorship W3217569112A5077063484 @default.
• W3217569112 hasAuthorship W3217569112A5083930081 @default.
• W3217569112 hasBestOaLocation W32175691121 @default.
• W3217569112 hasConcept C102230213 @default.
• W3217569112 hasConcept C104317684 @default.
• W3217569112 hasConcept C134018914 @default.
• W3217569112 hasConcept C141035611 @default.
• W3217569112 hasConcept C142724271 @default.
• W3217569112 hasConcept C169760540 @default.
• W3217569112 hasConcept C203014093 @default.
• W3217569112 hasConcept C204232928 @default.
• W3217569112 hasConcept C2776752467 @default.
• W3217569112 hasConcept C2776925932 @default.
• W3217569112 hasConcept C2777615887 @default.
• W3217569112 hasConcept C2777981454 @default.
• W3217569112 hasConcept C2779134260 @default.
• W3217569112 hasConcept C2779965356 @default.
• W3217569112 hasConcept C2780596555 @default.
• W3217569112 hasConcept C2780775167 @default.
• W3217569112 hasConcept C2985495968 @default.
• W3217569112 hasConcept C4224716 @default.
• W3217569112 hasConcept C529278444 @default.
• W3217569112 hasConcept C55493867 @default.
• W3217569112 hasConcept C71924100 @default.
• W3217569112 hasConcept C86803240 @default.
• W3217569112 hasConcept C95444343 @default.
• W3217569112 hasConceptScore W3217569112C102230213 @default.
• W3217569112 hasConceptScore W3217569112C104317684 @default.
• W3217569112 hasConceptScore W3217569112C134018914 @default.
• W3217569112 hasConceptScore W3217569112C141035611 @default.
• W3217569112 hasConceptScore W3217569112C142724271 @default.
• W3217569112 hasConceptScore W3217569112C169760540 @default.
• W3217569112 hasConceptScore W3217569112C203014093 @default.

• next