anti cathepsin d ctsd antibodies (Proteintech)

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Proteintech anti cathepsin d ctsd antibodies

Baicalein enhances autophagy after spinal cord ischemia-reperfusion injury (SCIR). (A) Immunofluorescence staining for LC3II and NeuN colocalization at the spinal cord lesion after SCIR (Scan bar = 25μm). (B) Immunofluorescence staining for p62 and NeuN colocalization at the spinal cord lesion after SCIR (Scan bar = 25μm). (C) The quantitative percentage of the LC3II positive neurons at the spinal cord lesion in each group. (D) The quantitative percentage of the p62 positive neurons in each group. (E) Western blotting for Beclin1, ATG5, VPS34, <t>CTSD,</t> ATP6V1B2, LC3II, and p62 expression levels in the Sham, SCIR+Vehicle, and SCIR+Baicalein groups. The gels were run under the same experimental conditions, and the cropped blots are shown here. (F) The optical density values of the Beclin1, ATG5, VPS34, CTSD, ATP6V1B2, LC3II, and p62 expression levels were quantified and analyzed in each group. The values are expressed as the means ± SEM, n=5 per group. * p < 0.05 and ** p < 0.01, vs. Sham group. ## p < 0.01, vs. SCIR+Vehicle group.

Anti Cathepsin D Ctsd Antibodies, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 72 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cpsd+function+of/Cathepsin+D+Antibody/pmc07438740-50-6-14
Average 95 stars, based on 72 article reviews

anti cathepsin d ctsd antibodies - by Bioz Stars, 2026-09

95/100 stars

Images

1) Product Images from "Baicalein Attenuates Pyroptosis and Endoplasmic Reticulum Stress Following Spinal Cord Ischemia-Reperfusion Injury via Autophagy Enhancement"

Article Title: Baicalein Attenuates Pyroptosis and Endoplasmic Reticulum Stress Following Spinal Cord Ischemia-Reperfusion Injury via Autophagy Enhancement

Journal: Frontiers in Pharmacology

doi: 10.3389/fphar.2020.01076

Figure Legend Snippet: Baicalein enhances autophagy after spinal cord ischemia-reperfusion injury (SCIR). (A) Immunofluorescence staining for LC3II and NeuN colocalization at the spinal cord lesion after SCIR (Scan bar = 25μm). (B) Immunofluorescence staining for p62 and NeuN colocalization at the spinal cord lesion after SCIR (Scan bar = 25μm). (C) The quantitative percentage of the LC3II positive neurons at the spinal cord lesion in each group. (D) The quantitative percentage of the p62 positive neurons in each group. (E) Western blotting for Beclin1, ATG5, VPS34, CTSD, ATP6V1B2, LC3II, and p62 expression levels in the Sham, SCIR+Vehicle, and SCIR+Baicalein groups. The gels were run under the same experimental conditions, and the cropped blots are shown here. (F) The optical density values of the Beclin1, ATG5, VPS34, CTSD, ATP6V1B2, LC3II, and p62 expression levels were quantified and analyzed in each group. The values are expressed as the means ± SEM, n=5 per group. * p < 0.05 and ** p < 0.01, vs. Sham group. ## p < 0.01, vs. SCIR+Vehicle group.

Techniques Used: Immunofluorescence, Staining, Western Blot, Expressing

Inhibition of autophagy reverses the effects of baicalein on endoplasmic reticulum (ER) stress, pyroptosis, and functional recovery after SCIR. (A) Western blotting for the Beclin1, ATG5, VPS34, CTSD, ATP6V1B2, LC3II and p62 expression levels in the SCIR+Baicalein, and SCIR+3MA groups. The gels were run under the same experimental conditions, and the cropped blots are shown here. (B) The optical density values of the Beclin1, ATG5, VPS34, CTSD, ATP6V1B2, LC3II and p62 expression levels were quantified and analyzed in each group. (C, D) Western blotting for the NLRP3, GSDMD, C-CASP1, GRP78, PDI, ATF4, CHOP, and CASP12 expression levels in the SCIR+Baicalein and SCIR+3MA groups. The gels were run under the same experimental conditions, and the cropped blots are shown here. (E, F) The optical density values of GRP78, PDI, ATF4, CHOP, CASP12, NLRP3, GSDM, and C-CASP1expression levels were quantified and analyzed in the both groups. (G, H) Enzyme-linked immunosorbent assay (ELISA) results for IL1βand IL18 expression levels in the SCIR+Baicalein and SCIR+3MA groups. (I, J) The BMS scores of the mice in each group at 24 h and 7 days after SCIR. The values are expressed as the means ± SEM, n=5 per group. * p < 0.05 and ** p < 0.01, vs. SCIR+Baicalein group.

Figure Legend Snippet: Inhibition of autophagy reverses the effects of baicalein on endoplasmic reticulum (ER) stress, pyroptosis, and functional recovery after SCIR. (A) Western blotting for the Beclin1, ATG5, VPS34, CTSD, ATP6V1B2, LC3II and p62 expression levels in the SCIR+Baicalein, and SCIR+3MA groups. The gels were run under the same experimental conditions, and the cropped blots are shown here. (B) The optical density values of the Beclin1, ATG5, VPS34, CTSD, ATP6V1B2, LC3II and p62 expression levels were quantified and analyzed in each group. (C, D) Western blotting for the NLRP3, GSDMD, C-CASP1, GRP78, PDI, ATF4, CHOP, and CASP12 expression levels in the SCIR+Baicalein and SCIR+3MA groups. The gels were run under the same experimental conditions, and the cropped blots are shown here. (E, F) The optical density values of GRP78, PDI, ATF4, CHOP, CASP12, NLRP3, GSDM, and C-CASP1expression levels were quantified and analyzed in the both groups. (G, H) Enzyme-linked immunosorbent assay (ELISA) results for IL1βand IL18 expression levels in the SCIR+Baicalein and SCIR+3MA groups. (I, J) The BMS scores of the mice in each group at 24 h and 7 days after SCIR. The values are expressed as the means ± SEM, n=5 per group. * p < 0.05 and ** p < 0.01, vs. SCIR+Baicalein group.

Techniques Used: Inhibition, Functional Assay, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

CMC:

Article Title: Da-Bu-Yin-Wan rescues cognitive deficits in aging and Alzheimer's disease models by Wnt/β-catenin-dependent restoration of lysosomal acidification.
Article Snippet: Background: Lysosomal acidification deficits are increasingly recognized as a convergent pathological mechanism driving both age-related cognitive decline (ARCD) and early Alzheimer's disease (AD) progression, creating a selfreinforcing cycle of cellular aging and Aβ dyshomeostasis.. Despite demonstrated neuroprotective effects of DaBu-Yin-Wan (DBYW) in Parkinson's disease models, its therapeutic potential for lysosomal dysfunction in ARCD and AD remains an uncharted area of investigation.. Purpose: This present work aimed to elucidate the mechanistic basis by which DBYW mitigates both ARCD and AD pathology through functionally rescuing impaired lysosomal acidification.

Polymer:

Staining:

Incubation:

Article Title: Disruption of FGL2 induces TFEB-dependent lysosomal degradation of PD-L1 and enhances the efficacy of anti-PD1 therapy in hepatocellular carcinoma
Article Snippet: .. Next, membranes were incubated with the following antibodies: FGL2 (1:500) (sc-100276, Santa Cruz Biotechnology), PD-L1 (1:4000) (66248-1-Ig, Proteintech), DDDDK-Tag (1:5000) (AE063, Abclonal), LAMP1 (1:10000) (67300-1-Ig, Proteintech), CTSD (1:10000) (21327-1-AP, Proteintech), TFEB (1:5000) (68632-1-Ig, Proteintech), phospho-TFEB (1:1000) (37681, CST), TFE3 (1:500) (A7936, Abclonal), MITF (1:1000) (13092-1-AP, Proteintech), GAPDH (1:50000) (60004-1-Ig, Proteintech), Histone H3 (1:5000) (17168-1-AP, Proteintech), p70S6K (1:1000) (2708, CST), phospho-p70S6K (1:1000) (9234, CST), 4EBP1 (1:1000) (9644, CST), phospho-4EBP1 (1:1000) (2855, CST), AKT (1:1000) (9272, CST), phospho-AKT (1:1000) (4060, CST), GSK3β(1:1000) (12456, CST), phospho-GSK3β (1:1000) (5558, CST), PKC (1:4000) (12919-1-AP, Proteintech), phospho-PKC (1:1000) (38938, CST), ERK1/2 (1:1000) (16443-1-AP, Proteintech), phospho-p44/42 MAPK (Erk1/2) (1:2000) (4370, CST), ATG5 (1:2000) (10181-2-AP, Proteintech), ATG7 (1:1000) (10088-2-AP, Proteintech), HRP goat anti-rabbit IgG (1:10000) (A21020, Abbkine) and HRP goat anti-mouse IgG (1:10000) (A21010, Abbkine). ..

Electrophoresis:

Article Title: Microglial Extracellular Vesicles Mediate C1q Deposition at the Pre‐Synapse and Promote Synaptic Pruning
Article Snippet: .. Proteins were then separated by electrophoresis, blotted on nitrocellulose membrane and probed for the following antibodies: mouse anti‐Lamp1 (1:1000, Invitrogen, cat.14‐1071‐85); rat anti‐CD68 (1:500, Biolegend, cat. 137001 clone FA‐11); rabbit anti‐Cathepsin D (1:400, Custom); mouse anti‐Tmem119 (1:500, Proteintech, cat.66984‐1‐IG); rabbit anti‐C3 (1:500, Abcam, cat. Ab200999 ); rabbit anti‐C1qA (1:500, Invitrogen, cat.PA5‐29586); rabbit anti‐Alix (1:500, Covalab, cat.PAB0204‐0X); mouse anti‐Flotillin (1:1000, BD Biosciences, cat.610820); rabbit anti‐Annexin A2 (1:5000, Abcam, cat.ab418003); mouse anti‐GS28 (1:1000, BD Bioscience, cat. 611184); rabbit anti‐GAPDH (1:1000, Synaptic Systems, cat. 347002); rabbit anti‐Iba‐1 (1:500, Wako, cat. 016–20001); mouse anti‐ALDH1L1 (1:500, Millipore, cat. MABN495); mouse anti‐GFAP (1:1000, Merck, cat. G3893); mouse anti‐L1CAM (1:500, Invitrogen, cat. 14‐1719‐83); mouse anti‐βIII‐tubulin (1:2000, Biolegend, cat. MMS‐435P); rabbit anti‐PLP (1:500, Merck, cat. SAB2101830); rabbit anti‐VGLUT1 (1:5000, Synaptic Systems, cat. 135 303); rabbit anti‐GM130 [1:1000, kindly provided by Dr M. Renz from the Institute of Immunology and Molecular Genetics, Karlsruhe, Germany (Seelig et al. )] and rabbit anti‐Tom‐20 (1:500, Santa Cruz Biotechnology, cat.sc‐11415). .. Photographic development was by chemiluminescence (ECL, Euroclone; Westar One Plus, Cyanagen; FEMTO, Thermo Fisher Scientific; or Westar Hypernova, Cyanagen) according to the manufacturer's instructions.

Membrane:

Article Title: Pathological axonal enlargement in connection with amyloidosis, lysosome destabilization, and bleeding is a major defect in Alzheimer’s disease
Article Snippet: .. The following primary antibodies and dilutions were used: Aβ (1:200, Abcam, Cambridge, UK, Cat# ab201061, RRID: AB_2722492), Aβ/AβPP (1:200, CST, Danvers, MA, USA, Cat# 2450, RRID: AB_490857), phos-tau (1:200, Abcam, Cat# ab151559, RRID: AB_2893278), microtubule associated protein 2 (MAP2; 1:200, Proteintech, Rosemont, IL, USA, Cat# 17490-1-AP, RRID: AB_2137880), apolipoprotein E (ApoE; 1:200, Abcam, Cat# ab183597, RRID: AB_3331650), Sortilin1 (1:200, Abcam, Cat# ab263864, RRID: AB_2884942), alpha-hemoglobin (HBA; 1:200, Abcam, Cat# ab92492, RRID: AB_10561594), Cathepsin D (1:200, Abcam, Cat# ab75852, RRID: AB_1523267), lysosome-associated membrane protein 2 (Lamp2; 1:100, Proteintech, Cat# 66301-1-Ig, RRID: AB_2881684), Cathepsin D (1:100, Proteintech, Cat# 66534-1-Ig, RRID: AB_2881897), glycosylated hemoglobin type A1C (HbA1c; 1:100, OkayBio, Nanjing, Jiangsu, China, Cat# K5a2), hemin (1:100, Absolute Antibody, Redcar, UK, Cat# 1D3), advanced glycation end products (AGE; 1:200, Abcam, Cat# ab23722, RRID: AB_447638), collagen type IV (ColIV; 1:200, Abcam, Cat# ab236640), and smooth muscle actin alpha 2 (ACTA2; 1:400, Proteintech, Cat# 23081-1-AP, RRID: AB_2815024). .. We used the following secondary antibodies and dilutions: donkey anti-mouse Alexa Fluor 594 secondary antibody (1:400, Jackson ImmunoResearch, West Grove, PA, USA, Cat# 715-585-150, RRID: AB_2340854), donkey anti-rabbit Alexa Fluor 488 secondary antibody (1:400, Jackson ImmunoResearch, Cat# 711-545-152, RRID: AB_2313584), donkey anti-rabbit Alexa Fluor 594 secondary antibody (1:400, Jackson ImmunoResearch, Cat# 711-585-152, RRID: AB_2340621), and donkey anti-mouse Alexa Fluor 488 secondary antibody (1:400, Jackson ImmunoResearch, Cat# 715-545-150, RRID: AB_2340846).

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