rab9 (Santa Cruz Biotechnology)
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Santa Cruz Biotechnology
rab9
Rab9, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rab9/Rab+9+siRNA/pm41274424-80-8-12
Average 93 stars, based on 6 article reviews
Rab9, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rab9/Rab+9+siRNA/pm41274424-80-8-12
Average 93 stars, based on 6 article reviews
rab9 - by Bioz Stars,
2026-10
93/100 stars
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Blocking Assay:Article Title: Decreased SREBP2 of the striatal cell relates to disrupted protein degradation in Huntington's disease. Article Snippet: This study delineated the intricate relation between cholesterol metabolism, protein degradation mechanisms, and the pathogenesis of Huntington’s disease (HD).. Through investigations using both animal models and cellular systems, we have observed significant alterations in cholesterol levels, particularly in the striatum, which is the primary lesion site in HD.. Our findings indicate the dysregulation of cholesterol metabolism-related factors, such as LDLR and SREBP2, in HD, which may contribute to disease progression. Knockdown:Article Title: Disruption of Rab9-dependent mitophagy contributes to menopause-induced sarcopenia. Article Snippet: .. For Rab9 RNA knockdown, cells were transfected with Article Title: Association of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 With Angiotensin II Type 1 Receptor Impacts Mitochondrial Quality Control, Offering Promise for the Treatment of Vascular Senescence Article Snippet: .. For ERK1, ERK2, and Rab9 RNA knockdown, cells were transfected with ERK1, ERK2, Article Title: Estrogen Plays a Crucial Role in Rab9‐Dependent Mitochondrial Autophagy, Delaying Arterial Senescence Article Snippet: .. For Rab9 RNA knockdown, cells were transfected with Transfection:Article Title: Disruption of Rab9-dependent mitophagy contributes to menopause-induced sarcopenia. Article Snippet: .. For Rab9 RNA knockdown, cells were transfected with Article Title: Association of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 With Angiotensin II Type 1 Receptor Impacts Mitochondrial Quality Control, Offering Promise for the Treatment of Vascular Senescence Article Snippet: .. For ERK1, ERK2, and Rab9 RNA knockdown, cells were transfected with ERK1, ERK2, Article Title: Estrogen Plays a Crucial Role in Rab9‐Dependent Mitochondrial Autophagy, Delaying Arterial Senescence Article Snippet: .. For Rab9 RNA knockdown, cells were transfected with Control:Article Title: Disruption of Rab9-dependent mitophagy contributes to menopause-induced sarcopenia. Article Snippet: .. For Rab9 RNA knockdown, cells were transfected with Article Title: Association of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 With Angiotensin II Type 1 Receptor Impacts Mitochondrial Quality Control, Offering Promise for the Treatment of Vascular Senescence Article Snippet: .. For ERK1, ERK2, and Rab9 RNA knockdown, cells were transfected with ERK1, ERK2, Article Title: Estrogen Plays a Crucial Role in Rab9‐Dependent Mitochondrial Autophagy, Delaying Arterial Senescence Article Snippet: .. For Rab9 RNA knockdown, cells were transfected with Polyacrylamide Gel Electrophoresis:Article Title: Variants in Miro1 Cause Alterations of ER-Mitochondria Contact Sites in Fibroblasts from Parkinson’s Disease Patients Article Snippet: Immortalized fibroblasts were lysed in RIPA buffer with 1× complete protease inhibitor (Roche, Mannheim, Germany). .. Sodium dodecyl sulfate polyacrylamide gel electrophoresis and Western blot analysis was performed using antibodies against Miro1 (Sigma Aldrich, Munich, Germany, WH0055288M1), Tom20 (Santa Cruz Biotechnologies, Dallas, TX, USA, sc-17764), Article Title: Variants in Miro1 Cause Alterations of ER-Mitochondria Contact Sites in Fibroblasts from Parkinson's Disease Patients. Article Snippet: Immortalized fibroblasts were lysed in RIPA buffer with 1× complete protease inhibitor (Roche, Mannheim, Germany). .. Sodium dodecyl sulfate polyacrylamide gel electrophoresis and Western blot analysis was performed using antibodies against Miro1 (Sigma Aldrich, Munich, Germany, WH0055288M1), Tom20 (Santa Cruz Biotechnologies, Dallas, TX, USA, sc-17764), Western Blot:Article Title: Variants in Miro1 Cause Alterations of ER-Mitochondria Contact Sites in Fibroblasts from Parkinson’s Disease Patients Article Snippet: Immortalized fibroblasts were lysed in RIPA buffer with 1× complete protease inhibitor (Roche, Mannheim, Germany). .. Sodium dodecyl sulfate polyacrylamide gel electrophoresis and Western blot analysis was performed using antibodies against Miro1 (Sigma Aldrich, Munich, Germany, WH0055288M1), Tom20 (Santa Cruz Biotechnologies, Dallas, TX, USA, sc-17764), Article Title: Variants in Miro1 Cause Alterations of ER-Mitochondria Contact Sites in Fibroblasts from Parkinson's Disease Patients. Article Snippet: Immortalized fibroblasts were lysed in RIPA buffer with 1× complete protease inhibitor (Roche, Mannheim, Germany). .. Sodium dodecyl sulfate polyacrylamide gel electrophoresis and Western blot analysis was performed using antibodies against Miro1 (Sigma Aldrich, Munich, Germany, WH0055288M1), Tom20 (Santa Cruz Biotechnologies, Dallas, TX, USA, sc-17764), Article Title: Mutations in RHOT1 Disrupt Endoplasmic Reticulum–Mitochondria Contact Sites Interfering with Calcium Homeostasis and Mitochondrial Dynamics in Parkinson's Disease Article Snippet: Fibroblasts were lysed in RIPA buffer containing 1 × complete protease inhibitor (Roche). .. Western blot analysis was performed with antibodies against Miro1 (WH0055288M1; Sigma–Aldrich, Munich, Germany), LC3-I/II (2775; Cell Signaling), Hsp60 (4870; Cell Signaling), Tom20 (sc-17764; Santa Cruz Biotechnologies), |
![(a–f) U2OS cells (wild-type [WT], ULK1/2 double knockout [DKO], ATG7 knockout [KO], or <t>RAB9</t> KO were transfected with the E-cadherin RUSH construct. After 48 h, cells were incubated in Dulbecco’s Modified Eagle Medium (DMEM) with or without glucose for 1 h, followed by biotin treatment for 30 min. ( a ) Representative immunofluorescence images captured following anti-GM130 and DAPI staining show changes in reporter distribution after biotin addition and/or glucose starvation. ( b ) Percentage of cells (mean ± S.E.M., n = 3 biological replicates, >37 cells per replicate) with Golgi-localized E-cadherin. ( c–f ) Representative immunoblot analyses show protein levels of ULK1, ULK2, ATG7, or RAB9 in WT and indicated KO cell lines; * indicates nonspecific band in ( e ). ( g–i ) Rescue of glucose starvation–induced ER-to-Golgi trafficking inhibition was evaluated in U2OS ULK1/2 DKO cells stably expressing empty vector (EV), WT ULK1, kinase-dead ULK1 (K46A), or AMPK-resistant ULK1 (4SA). Cells were transfected with the E-cadherin RUSH construct, incubated in DMEM with or without glucose for 1 h, and treated with biotin for 30 min. ( g ) Representative immunofluorescence images captured following anti-GM130 and DAPI staining show changes in reporter distribution after biotin addition and/or glucose starvation. ( h ) Golgi-localized E-cadherin in U2OS ULK1/2 DKO cells expressing WT or mutant forms of ULK (mean ± S.E.M., n = 3 biological replicates, >30 cells per replicate). ( i ) Representative immunoblot analysis shows AMPK activity as indicated by total and phospho-ACC, and ULK1 expression, and AMPK-mediated phosphorylation of ULK1 at S555 in the indicated cell lines. ( j–l ) WT U2OS cells were transfected with the E-cadherin RUSH construct. After 48 h, cells were pre-treated with compound C (5 μM, 4 h) or MRT68921 (1 μM, 24 h) and incubated in DMEM with or without glucose for 1 h, followed by biotin treatment for 30 min. ( j ) Representative immunofluorescence images following anti-GM130 and DAPI staining show changes in reporter distribution after biotin addition and/or glucose starvation. ( k ) Golgi-localized E-cadherin in U2OS cells before and after glucose starvation (mean ± S.E.M., n = 3 biological replicates, >103 cells per replicate). ( l ) Representative immunoblot analysis demonstrates activity of each inhibitor post biotin treatment. ( m–o ) WT or Prkaa1/2 (AMPKα1/2) DKO murine embryonic fibroblasts (MEFs) were transfected with the E-cadherin RUSH construct. After 48 h, cells were incubated in DMEM with or without glucose for 1 h, followed by biotin treatment for 30 min. ( m ) Representative immunofluorescence images captured following anti-GM130 and DAPI staining show changes in reporter distribution after biotin addition and/or glucose starvation. ( n ) Golgi-localized E-cadherin in in WT and AMPK α1/2 DKO MEFs before and after glucose starvation (mean ± S.E.M., n = 3 biological replicates, >33 cells per replicate). ( o ) Levels of phosphorylated ACC and ULK1 in WT and AMPK α1/2 DKO MEFs after 1-h glucose starvation. Statistical significance was analyzed with one-way ANOVA followed by Tukey’s multiple comparisons. ***P < 0.001, **P < 0.01, *P < 0.05; ns, not significant. Scale bar, 10 μm.](https://bio-rxiv-images-cdn.bioz.com/dois_ending_with_04/10__1101_slash_2025__10__31__685804/10__1101_slash_2025__10__31__685804___F7.large.jpg)