Central nervous system specific high molecular weight ALS2/alsin homophilic complex is enriched in mouse brain synaptosomes

• 資料種別: 記事
• タイトル: Central nervous system specific high molecular weight ALS2/alsin homophilic complex is enriched in mouse brain synaptosomes
• 著者標目: Kai Sato; Kyoko Suzuki-Utsunomiya; Shun Mitsui; Suzuka Ono; Kento Shimakura; Asako Otomo; Shinji Hadano
• 出版年月日等: 2023-01
• 出版年（W3CDTF）: 2023-01
• タイトル（掲載誌）: Biochemical and Biophysical Research Communications
• 巻号年月日等（掲載誌）: 638
• 掲載巻: 638
• 掲載ページ: 168-175
• 掲載年月日（W3CDTF）: 2023-01
• ISSN（掲載誌）: 0006291X
• 出版事項（掲載誌）: Elsevier BV
• 件名標目: Central Nervous System; Amyotrophic Lateral Sclerosis; Brain; Endosomes; Molecular Weight; Mice; Animals; Guanine Nucleotide Exchange Factors; Synaptosomes
• 対象利用者: 一般
• 標準番号（その他）: PMID : 36459881
• DOI: 10.1016/j.bbrc.2022.11.061; https://doi.org/10.1016/j.bbrc.2022.11.061
• 作成日（W3CDTF）: 2022-11-22
• 著作権情報: https://www.elsevier.com/tdm/userlicense/1.0/; https://www.elsevier.com/legal/tdmrep-license; http://creativecommons.org/licenses/by-nc/4.0/
• 関連情報（URI）: https://api.elsevier.com/content/article/PII:S0006291X22016102?httpAccept=text/xml; https://api.elsevier.com/content/article/PII:S0006291X22016102?httpAccept=text/plain
• 参照: Genetic background and gender effects on gross phenotypes in congenic lines of ALS2/alsin-deficient mice; https://cir.nii.ac.jp/crid/1360004232393433984; HEREDITARY MOTOR SYSTEM DISEASES (CHRONIC JUVENILE AMYOTROPHIC LATERAL SCLEROSIS); https://cir.nii.ac.jp/crid/1360011146145328768; Defective relocalization of ALS2/alsin missense mutants to Rac1-induced macropinosomes accounts for loss of their cellular function and leads to disturbed amphisome formation; https://cir.nii.ac.jp/crid/1360286437279765376; Homo-oligomerization of ALS2 through Its Unique Carboxyl-terminal Regions Is Essential for the ALS2-associated Rab5 Guanine Nucleotide Exchange Activity and Its Regulatory Function on Endosome Trafficking; https://cir.nii.ac.jp/crid/1360292619486259072; The gene encoding alsin, a protein with three guanine-nucleotide exchange factor domains, is mutated in a form of recessive amyotrophic lateral sclerosis; https://cir.nii.ac.jp/crid/1360292620582031360; The N-terminal intrinsically disordered region mediates intracellular localization and self-oligomerization of ALS2; https://cir.nii.ac.jp/crid/1360294643763758464; Altered oligomeric states in pathogenic ALS2 variants associated with juvenile motor neuron diseases cause loss of ALS2-mediated endosomal function; https://cir.nii.ac.jp/crid/1360294647777547648; Rab5 and Alsin regulate stress-activated cytoprotective signaling on mitochondria; https://cir.nii.ac.jp/crid/1360298764640111360; ALS2, the small GTPase Rab17-interacting protein, regulates maturation and sorting of Rab17-associated endosomes; https://cir.nii.ac.jp/crid/1360568466625221632; ALS2/Alsin Regulates Rac-PAK Signaling and Neurite Outgrowth; https://cir.nii.ac.jp/crid/1360855568785122816; AI-based protein structure databases have the potential to accelerate rare diseases research: AlphaFoldDB and the case of IAHSP/Alsin; https://cir.nii.ac.jp/crid/1360861704761027072; Prediction of Protein–Protein Interactions Between Alsin DH/PH and Rac1 and Resulting Protein Dynamics; https://cir.nii.ac.jp/crid/1360861710911410176; ALS2 regulates endosomal trafficking, postsynaptic development, and neuronal survival; https://cir.nii.ac.jp/crid/1360861711383213312; Loss of ALS2/Alsin Exacerbates Motor Dysfunction in a SOD1H46R-Expressing Mouse ALS Model by Disturbing Endolysosomal Trafficking; https://cir.nii.ac.jp/crid/1361412342635024768; Absence of alsin function leads to corticospinal motor neuron vulnerability via novel disease mechanisms; https://cir.nii.ac.jp/crid/1361418518798811136; Unstable mutants in the peripheral endosomal membrane component ALS2 cause early-onset motor neuron disease; https://cir.nii.ac.jp/crid/1361418518995428224; ALS2, a novel guanine nucleotide exchange factor for the small GTPase Rab5, is implicated in endosomal dynamics; https://cir.nii.ac.jp/crid/1361418520174401152; ALS2/alsin deficiency in neurons leads to mild defects in macropinocytosis and axonal growth; https://cir.nii.ac.jp/crid/1361981469315404800; Alsin and SOD1G93A Proteins Regulate Endosomal Reactive Oxygen Species Production by Glial Cells and Proinflammatory Pathways Responsible for Neurotoxicity; https://cir.nii.ac.jp/crid/1361981469426369408; Molecular interaction of neurocalcin α with alsin (ALS2); https://cir.nii.ac.jp/crid/1362544419197547136; Mice deficient in the Rab5 guanine nucleotide exchange factor ALS2/alsin exhibit age-dependent neurological deficits and altered endosome trafficking; https://cir.nii.ac.jp/crid/1363107370326680832; The Rab5 Activator ALS2/alsin Acts as a Novel Rac1 Effector through Rac1-activated Endocytosis; https://cir.nii.ac.jp/crid/1363388844757010560; ALS2CL, a novel ALS2-interactor, modulates ALS2-mediated endosome dynamics; https://cir.nii.ac.jp/crid/1363951794825384192; A gene encoding a putative GTPase regulator is mutated in familial amyotrophic lateral sclerosis 2; https://cir.nii.ac.jp/crid/1364233269430765952
• 連携機関・データベース: 国立情報学研究所 : CiNii Research; https://cir.nii.ac.jp/
• 提供元機関・データベース: Crossref; https://www.crossref.org; 科学研究費助成事業データベース; https://kaken.nii.ac.jp/ja

• 要約等: ALS2/alsin, the causative gene product for a number of juvenile recessive motor neuron diseases, acts as a guanine nucleotide exchange factor (GEF) fo...