Journal: Zoological Research

Article Title: Comparative analysis of primate and pig cells reveals primate-specific PINK1 expression and phosphorylation

doi: 10.24272/j.issn.2095-8137.2023.241

Figure Lengend Snippet: Undetectable PINK1 in pig tissues using antibodies targeting middle region of PINK1

Article Snippet: Additionally, a synthetic peptide containing the pig PINK1 protein sequences (residues 484–504) was used as an antigen to produce a rabbit polyclonal antibody (anti-pig PINK1) by Boster Biological Technology (China).

Techniques:

Journal: Zoological Research

Article Title: Comparative analysis of primate and pig cells reveals primate-specific PINK1 expression and phosphorylation

doi: 10.24272/j.issn.2095-8137.2023.241

Figure Lengend Snippet: Undetectable PINK1 in pig tissues using antibodies targeting C-terminal region of PINK1

Article Snippet: Additionally, a synthetic peptide containing the pig PINK1 protein sequences (residues 484–504) was used as an antigen to produce a rabbit polyclonal antibody (anti-pig PINK1) by Boster Biological Technology (China).

Techniques:

Journal: Zoological Research

Article Title: Comparative analysis of primate and pig cells reveals primate-specific PINK1 expression and phosphorylation

doi: 10.24272/j.issn.2095-8137.2023.241

Figure Lengend Snippet: PINK1 mRNA expression in different species

Article Snippet: Additionally, a synthetic peptide containing the pig PINK1 protein sequences (residues 484–504) was used as an antigen to produce a rabbit polyclonal antibody (anti-pig PINK1) by Boster Biological Technology (China).

Techniques: Expressing

Journal: Zoological Research

Article Title: Comparative analysis of primate and pig cells reveals primate-specific PINK1 expression and phosphorylation

doi: 10.24272/j.issn.2095-8137.2023.241

Figure Lengend Snippet: PINK1 mRNA expression in pig tissues and siRNA-mediated knockdown in cultured astrocytes

Article Snippet: Additionally, a synthetic peptide containing the pig PINK1 protein sequences (residues 484–504) was used as an antigen to produce a rabbit polyclonal antibody (anti-pig PINK1) by Boster Biological Technology (China).

Techniques: Expressing, Knockdown, Cell Culture

Journal: Zoological Research

Article Title: Comparative analysis of primate and pig cells reveals primate-specific PINK1 expression and phosphorylation

doi: 10.24272/j.issn.2095-8137.2023.241

Figure Lengend Snippet: Undetectable PINK1 in cultured pig astrocytes subjected to siRNA-mediated knockdown

Article Snippet: Additionally, a synthetic peptide containing the pig PINK1 protein sequences (residues 484–504) was used as an antigen to produce a rabbit polyclonal antibody (anti-pig PINK1) by Boster Biological Technology (China).

Techniques: Cell Culture, Knockdown

Journal: Zoological Research

Article Title: Comparative analysis of primate and pig cells reveals primate-specific PINK1 expression and phosphorylation

doi: 10.24272/j.issn.2095-8137.2023.241

Figure Lengend Snippet: Differential PINK1-mediated phosphorylation in monkey and pig brain tissues

Article Snippet: Additionally, a synthetic peptide containing the pig PINK1 protein sequences (residues 484–504) was used as an antigen to produce a rabbit polyclonal antibody (anti-pig PINK1) by Boster Biological Technology (China).

Techniques: Phospho-proteomics

Journal: The FASEB Journal

Article Title: Tmx2 Maintains Mitochondrial Function to Support Preimplantation Embryogenesis

doi: 10.1096/fj.202500640r

Figure Lengend Snippet: FIGURE 6 | Tmx2 knockdown inhibits mitophagy and autophagy in morula-stage embryos. (A-D) Immunostaining for PINK1 (A), PARKIN (B), MAP1LC3B (C), and LAMP1 (D) in control and Tmx2-knockdown embryos. Scale bars: 75 μm. (E-H) Quantification of immunofluorescence inten- sity for PINK1 (E), PARKIN (F), MAP1LC3B (G), and LAMP1 (H) in control and Tmx2-knockdown morula-stage embryos. Sample sizes: PINK1: Control = 16, siRNA2 = 14, siRNA3 = 19; PARKIN: Control = 21, siRNA2 = 20, siRNA3 = 23; MAP1LC3B: Control = 22, siRNA2 = 20, siRNA3 = 21; LAMP1: Control = 30, siRNA2 = 32, siRNA3 = 31. Statistical significance: **p < 0.01, ***p < 0.001 and ****p < 0.0001.

Article Snippet: The primary antibodies used included: rabbit anti- TMX2 (Origene, TA341391, 1:50), goat anti- OCT4 (Abcam, ab27985, 1:200), mouse antiCDX2 (Biogenex, MU392A- UC, 1:100), goat anti- SOX17 (R&D Systems, AF1924, 1:100), rabbit anti- NANOG (Abcam, ab80892, 1:50), rabbit anti- PINK1 (Affinity, DF7742, 1:50), rabbit antiPARKIN (Abcepta, AP6402B, 1:50), rabbit anti- MAP1LC3B (CUSABIO, CSB- PA013403GA01HU, 1:50), and rabbit antiLAMP1 (Beyotime, AF7353, 1:100).

Techniques: Knockdown, Immunostaining, Control, Immunofluorescence

Journal: Neurobiology of aging

Article Title: Loss of PINK1 causes age-dependent decrease of dopamine release and mitochondrial dysfunction

doi: 10.1016/j.neurobiolaging.2018.10.025

Figure Lengend Snippet: Representative traces for 1p-evoked DA release in dSTR slices from both WT and PINK1 KO mice using FSCV were showed for young group (A) and old group (C) respectively. No significant difference of 1p-evoked DA release was found between PINK1 KO and WT in the young group (B, N = 6, n = 15), whereas it was significantly decreased (~30 %) in PINK1 KO in the old group (D, N = 7, n = 22). (E) Representative trace for KCl-evoked total DA release, no significant KCl-evoked DA overflow was found in either young (F, N = 5, n = 19) or old group (G, N = 4, n = 19). (H) No degeneration of DA axon terminals in PINK1 KO mice in the old group. Left panel, representative images of DA axon terminals in the striatum from WT and KO mice labeled by TH; right panel, quantification of TH-labeled DA terminals as fraction of the striatum area (N = 3 for each genotype). * p < 0.05.

Article Snippet: Brain extracts from homozygous PINK1 KO mice was tested by RT-PCR and Western blot with anti-PINK1 antibody (A gift from Eli Lilly Inc.), and confirmed that PINK1 mRNA and protein were absent in the PINK1 KO mice ( Figure S1D and E ).

Techniques: Labeling

Journal: Neurobiology of aging

Article Title: Loss of PINK1 causes age-dependent decrease of dopamine release and mitochondrial dysfunction

doi: 10.1016/j.neurobiolaging.2018.10.025

Figure Lengend Snippet: Representative traces of 1p-evoked DA release were showed in WT and PINK1 KO mice in both young (A) and old group (D), before (black) and after cocaine treatment (Liu et al.). The young group of PINK1 KO mice did not show obvious decrease of DA release compared to WT controls in the presence of 5 μM cocaine (N = 6, n = 13) (B), whereas in the old group, the PINK1 KO mice showed 25 % less DA release compared to WT controls (E), at a similar decreased level as without DAT blockade (N = 4, n = 10). No significant difference in fold change of DA release were observed after cocaine treatment for PINK1 KO and WT slice in both young (C, N = 6, n = 13) and old group (F, N = 4, n = 10).

Article Snippet: Brain extracts from homozygous PINK1 KO mice was tested by RT-PCR and Western blot with anti-PINK1 antibody (A gift from Eli Lilly Inc.), and confirmed that PINK1 mRNA and protein were absent in the PINK1 KO mice ( Figure S1D and E ).

Techniques:

Journal: Neurobiology of aging

Article Title: Loss of PINK1 causes age-dependent decrease of dopamine release and mitochondrial dysfunction

doi: 10.1016/j.neurobiolaging.2018.10.025

Figure Lengend Snippet: Representative traces of FCCP induced DA massive release in dSTR slices from WT (A) and PINK1 KO (B) mice. The starting point of mass release did not show significant difference in the young group (C, N = 4, n = 8), whereas was significant earlier for the PINK1 KO slices in the old group (D, N = 4, n = 8). There was no significant alteration of FCCP induced mass DA release in either young (E) or old group (F). * P < 0.05.

Article Snippet: Brain extracts from homozygous PINK1 KO mice was tested by RT-PCR and Western blot with anti-PINK1 antibody (A gift from Eli Lilly Inc.), and confirmed that PINK1 mRNA and protein were absent in the PINK1 KO mice ( Figure S1D and E ).

Techniques:

Journal: Neurobiology of aging

Article Title: Loss of PINK1 causes age-dependent decrease of dopamine release and mitochondrial dysfunction

doi: 10.1016/j.neurobiolaging.2018.10.025

Figure Lengend Snippet: OCRs of acute STR slices (150 μm*1.5 mm) from both the young (A, B, and C) and the old group (D, E, and F) mice, exposed to successive additions of respiratory modulators (showed in arrows). OCR of the young group was not significantly different between different genotype (B), while the coupling efficiency was decreased in PINK1 KO slices (C). In the old group, the PINK1 KO slices showed significantly decrease of basal respiration level (E) and the coupling efficiency (F). With 10 mM pyruvate (P), 20 μM Oligomycin (O), 10 μM FCCP (F), and 20 μM Antimycin A (A) injected sequentially. N = 4 for each genotype and age.

Article Snippet: Brain extracts from homozygous PINK1 KO mice was tested by RT-PCR and Western blot with anti-PINK1 antibody (A gift from Eli Lilly Inc.), and confirmed that PINK1 mRNA and protein were absent in the PINK1 KO mice ( Figure S1D and E ).

Techniques: Injection

Journal: Neurobiology of aging

Article Title: Loss of PINK1 causes age-dependent decrease of dopamine release and mitochondrial dysfunction

doi: 10.1016/j.neurobiolaging.2018.10.025

Figure Lengend Snippet: Bar graph showing lower ATP levels in PINK1 KO striatal slices compared to WT in the old age group (N = 7 for each genotype, * P < 0.05). ATP levels were not altered in the young age group (N = 4 for each genotype).

Article Snippet: Brain extracts from homozygous PINK1 KO mice was tested by RT-PCR and Western blot with anti-PINK1 antibody (A gift from Eli Lilly Inc.), and confirmed that PINK1 mRNA and protein were absent in the PINK1 KO mice ( Figure S1D and E ).

Techniques:

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Pink1/PARK2/mROS-Dependent Mitophagy Initiates the Sensitization of Cancer Cells to Radiation

doi: 10.1155/2021/5595652

Figure Lengend Snippet: Sarm1-mtKR-induced mtROS participated in the autophagic cell death depending on the Pink1/PARK2 pathway. (a) WB was performed to determine protein levels of Pink1, PARK2, and Tom20 in total- and mito-proteins. GAPDH and HSP60 proteins were used for loading control. (b) The gray ratios of Pink1, PARK2, and Tom20 in total- and mito-proteins. (c) Pink1 and Tom20 mRNAs detected by qRT-PCR. Bars represent mean ± SD of triplicate measurements. ∗ P < 0.05 and ∗∗ P < 0.01, versus control; # P < 0.05, versus light exposure.

Article Snippet: Anti-COX IV, anti- β -actin, and anti-GAPDH were purchased from Santa Cruz, CA, USA; anti-voltage-dependent anion channel 1 (VDAC1), anti-heat-shock protein 60 (HSP60), anti-Pink1, and anti-PARK2 were purchased from Bioworld Technology, Inc., USA; and anti-microtubule-associated protein 1 light chain 3 (LC3), anti-p62, and anti-Tom20 were purchased from Cell Signaling Technology, Danvers, MA, USA.

Techniques: Quantitative RT-PCR