FIS1 (E3K9O) Rabbit mAb 32525T from Cell Signaling Technology

Published Figures

Register or Sign In to View Figures.

Clinical and Translational Medicine
August 01 2024

Fig 1: Exogenous IL‐10 supplement reverses the aggravated ALI, macrophages metabolic alterations and polarisation caused by CPT1A deficiency in LPS‐stimulated model. (a) Exogenous rIL‐10 (45 µg/kg) was administrated to Cre+ CPT1A fl/fl mice simultaneously with LPS (10 mg/kg) challenge. After 24 h, mice were euthanised and Balf was collected and estimated for total cell number, macrophage, neutrophil, and lymphocyte numbers. n = 4 biologically independent samples. *p = .0133, ***p = .0006, **p = .0041. (b, c) Production of cytokines IFN‐γ, IL‐6, G‐CSF, and CXCL1/KC in Balf and serum was assessed via ELISA kits. n = 4 biologically independent samples. (b) ***p = .0002, ****p < .0001, **p = .0011, *p = .031. (c) **p = .0013, **p = .0017, ****p < .0001, *p = .0144. (d) Quantitative immunoblotting analysis indicating the protective effect of rIL‐10 on the NLRP3/Caspase‐1 activation for lung inflammation in Cre+ CPT1A fl/fl mice. n = 4 biologically independent samples. *p = .0272, **p = .0072. (e) Representative images of H&E‐stained lung tissue sections of Cre+ CPT1A fl/fl mice after LPS challenge with or without rIL‐10 treatment. Scale bars in the upper panel, 200 µm; scale bars in the lower panel, 50 µm. n = 4 biologically independent samples. ****p < .0001. (f) After LPS stimulation for 6 h with or without rIL‐10 pretreatment, the mRNA expressions of cytokines IL‐1β, IL‐18, IL‐6 and TNF‐α in Cre+ CPT1A fl/fl BMDMs were examined by qRT‐PCR. Data are expressed as fold change. n = 4 biologically independent samples. **p = .0021, *p = .0206, *p = .0157. (g) Quantitative immunoblotting analysis showing the effect of rIL‐10 on the NLRP3/Caspase‐1 activation for macrophage inflammation after 24 h of LPS stimulation. n = 4 biologically independent samples. NLRP3, *p = .0166, Caspase‐1 p10, *p = .0145. (h) Confocal microscopy images showing the mitochondrial mass of BMDMs from each group using MitoTracker probe. Scale bars, 20 µm. (i) Microplate reader assay exhibiting the effect of rIL‐10 on mitochondrial and intracellular ROS production induced by LPS in Cre+ CPT1A fl/fl BMDMs. n = 4 biologically independent samples. **p = .004. (j) Quantitative immunoblotting analysis indicating the effect of rIL‐10 on the expression of OPA1, MFN2, DRP1 and FIS1 for mitochondrial dynamics in Cre+ CPT1A fl/fl BMDMs. n = 4 biologically independent samples. OPA1, **p = .0082. MFN2, *p = .0124. DRP1, **p = .0032. FIS1, *p = .013. (k, l) Induction of LDHA, HIF‐1α and GLUT (k), as well as SCAP, SREBP and LDLr (l) mRNA expression in Cre+ CPT1A fl/fl BMDMs with or without rIL‐10 addition was estimated by qRT‐PCR. Data are expressed as fold change. n = 4 biologically independent samples. (k) HIF‐1α, ***p = .0002, GLUT, ****p < .0001. (l) SCAP, **p = .0029, SREBP, **p = .0053, LDLr, **p = .0029. (m) After 12 h treatment with LPS with or without rIL‐10 supplement in BMDMs, production of ATP, as well as intracellular FAO metabolites, citrate and acetyl CoA were measured. n = 4 biologically independent samples. ATP, *p = .0173. citrate, **p = .0011. Acetyl CoA, **p = .003. (n) Induction of iNOS, IL‐12, ARG1 and YM1 mRNA expression in Cre+ CPT1A fl/fl BMDMs was analysed via qRT‐PCR. Data are expressed as fold change. n = 4 biologically independent samples. iNOS, ***p = .0003. IL‐12, ****p < .0001. (o) Quantitative immunoblotting analysis verifying the effect of rIL‐10 on iNOS and ARG1 expression for macrophage polarisation in Cre+ CPT1A fl/fl BMDMs upon LPS challenge. n = 4 biologically independent samples. iNOS, *p = .0142. ARG1, *p = .0179. (p) The phagocytic capacity of Cre+ CPT1A fl/fl BMDMs with or without rIL‐10 treatment was evaluated by the pHrod Green E. coli BioParticles through both confocal microscopy (showed in the upper panel; scale bars, 20 µm) and fluorescence plate reader (showed in the lower panel). n = 4 biologically independent samples. ***p = .0002. Data are presented as mean ± SEM and analysed with a 95% confidence interval. p Values were calculated using unpaired Student's t‐test.
Register or Sign In to View Figures.

Clinical and Translational Medicine
August 01 2024

Fig 2: CPT1A regulates aberrant inflammation and mitochondrial stability in macrophages upon LPS challenge. (a) Schematic diagram of the extraction, separation and cultivation of BMDMs in vitro. Some figure elements were created with BioRender.com. (b) Macrophage CPT1A depletion was verified by immunoblotting in BMDMs from Cre− CPT1A fl/fl and Cre+ CPT1A fl/fl mice. n = 4 biologically independent samples. (c) After LPS stimulation (100 ng/mL) for 6 h, the induction of cytokines IL‐1β, IL‐18, IL‐6 and TNF‐α mRNA expression in each group was analysed by qRT‐PCR. Data are expressed as fold change. n = 6 biologically independent samples. ***p = .0007, ***p = .0004, ****p < .0001. (d, e) After LPS (100 ng/mL) treatment for 24 h, quantitative immunoblotting analysis indicating the effect of CPT1A expression on NLRP3/Caspase‐1 p10 level for inflammasome activation in BMDMs. n = 3 biologically independent samples. (d) ***p = .0002 (Cre− CPT1A fl/fl+Con group vs. Cre− CPT1A fl/fl+LPS group), ***p = .0001 (Cre− CPT1A fl/fl+Con group vs. Cre+ CPT1A fl/fl+Con group), *p = .0451 (Cre+ CPT1A fl/fl+Con group vs. Cre+ CPT1A fl/fl+LPS group), *p = .0243 (Cre− CPT1A fl/fl+LPS group vs. Cre+ CPT1A fl/fl+LPS group). (e) **p = .0015 (Cre− CPT1A fl/fl+Con group vs. Cre− CPT1A fl/fl+LPS group), *p = .0411, ***p = .0002, **p = .0023 (Cre− CPT1A fl/fl+LPS group vs. Cre+ CPT1A fl/fl+LPS group). (f, g) Microplate reader assay showing the effect of CPT1A on the production of mitochondrial (f) and intracellular ROS (g) induced by LPS (100 ng/mL) in BMDMs. n = 6 biologically independent samples. (f) *p = .0114 (Cre− CPT1A fl/fl+Con group vs. Cre− CPT1A fl/fl+LPS group), ***p = .0002, *p = .0243. (g) *p = .0268, ****p < .0001. (h) Confocal microscopy images showing the mitochondrial mass of BMDMs from each group using MitoTracker probe. Scale bars, 20 µm. (i–l) Quantitative immunoblotting analysis indicating the effect of CPT1A on the expression of OPA1, MFN2, DRP1 and FIS1 for mitochondrial dynamics in BMDMs. n = 6 biologically independent samples. (i) *p = .013 (Cre− CPT1A fl/fl+Con group vs. Cre− CPT1A fl/fl+LPS group), ***p = .0002 (Cre+ CPT1A fl/fl+Con group vs. Cre+ CPT1A fl/fl+LPS group), *p = .0397 (Cre− CPT1A fl/fl+LPS group vs. Cre+ CPT1A fl/fl+LPS group). (j) **p = .0026 (Cre− CPT1A fl/fl+Con group vs. Cre− CPT1A fl/fl+LPS group), **p = .0035 (Cre+ CPT1A fl/fl+Con group vs. Cre+ CPT1A fl/fl+LPS group). (k) **p = .0063 (Cre− CPT1A fl/fl+Con group vs. Cre− CPT1A fl/fl+LPS group), **p = .0028 (Cre− CPT1A fl/fl+LPS group vs. Cre+ CPT1A fl/fl+LPS group), ***p = .0004. (l) *p = .027 (Cre− CPT1A fl/fl+Con group vs. Cre+ CPT1A fl/fl+Con group), *p = .0154 (Cre+ CPT1A fl/fl+Con group vs. Cre+ CPT1A fl/fl+LPS group), **p = .0049. Data are presented as mean ± SEM and analysed with a 95% confidence interval. p Values were calculated using one‐way ANOVA followed by Bonferroni's post hoc test.
Register or Sign In to View Figures.

Chin Med
January 15 2025

Fig 3: Notoginsenoside R2 reversed mitochondrial dysfunction and apoptosis by suppressing c-Src in HK-2 cells. A Representative images of MitoSOX dyeing and semiquantitative analysis. B JC-1 staining performed by flow cytometry to evaluate the mitochondrial membrane potential of each group. C Western blot analysis for Drp1, Mfn2, and Fis1 expression in HK-2 cells. D MitoSOX semiquantitative analysis (n = 3). E Quantitative analysis of JC-1 (n = 3). F–H Quantitative analysis of Western blot (n = 3). I Representative images of TUNEL assay. J Annexin V-FITC/PI staining to measure apoptotic cells by flow cytometry. K Western blot analysis for Bcl-2, Bax, and cleaved-caspase-3 expression in HK-2 cells. L Semiquantitative analysis of TUNEL assay (n = 3). M Quantitative analysis of Annexin V-FITC/PI (n = 3). N–P Quantitative analysis of Western blot (n = 3). (*p < 0.05 and **p < 0.01 compared with normal control group; #p < 0.05 and ##p < 0.01 compared with HGPA model group; ns: no statistical difference compared with HGPA group)
Register or Sign In to View Figures.

International journal of molecular sciences
December 15 2023

Fig 4: Effect of Mfn2 overexpression on fusion and fission mediators, apoptosis, and proliferation in pulmonary arterial endothelial cells. PAECs were transduced with Ad-MFN2 (MOI = 5) or Ad-GFP, and Western blot analysis was used to confirm increased Mfn2 protein levels ((A), upper blot). The membrane was stripped and reprobed with an Mfn1 antibody to analyze the expression of Mfn1 protein. Overexpression of Mfn2 increased Mfn1 protein levels ((A), middle blot). Mfn2 overexpression did not affect the expression level of the fusion mediator Opa1 (B) or the fission mediators Drp1 (C) and Fis1 (D). Representative images are shown. β-actin was used to normalize protein loading. Mfn2 overexpression increased the aspect ratio (AR) in PAECs (E). TUNEL staining of PAECs identified increased apoptosis in MFN2-overexpressing PAECs (F). MFN2 overexpression also reduced the proliferation of PAECs (G). Data are mean ± SEM; n = 4–6. * p < 0.05 vs. control PAECs.
Register or Sign In to View Figures.

Clinical and Translational Medicine
August 01 2024

Fig 5: IL‐10 is essential in the restoration of ALI models, which could protect the anti‐inflammatory activities of macrophages from the mitochondrial dysfunction under LPS challenge. (a) WT and IL‐10−/− mice were administrated nasally with PBS or LPS (10 mg/kg) with or without rIL‐10 treatment (45 µg/kg). After 24 h, mice were euthanised and Balf was collected and estimated for total cell number, macrophage, neutrophil, and lymphocyte numbers. n = 6 biologically independent samples. Balf total cell, *p = .014 (WT+LPS group vs. IL‐10 −/−+LPS group), *p = .0114 (IL‐10 −/−+LPS group vs. IL‐10 −/−+rIL‐10+LPS group), **p = .0014 (WT+LPS group vs. WT+rIL‐10+LPS group), **p = .0018 (WT+rIL‐10+LPS group vs. IL‐10 −/−+rIL‐10+LPS group), ****p < .0001. Macrophage, *p = .0251, ***p = .0002, ****p < .0001. Neutrophil, **p = .0011 (WT+LPS group vs. WT+rIL‐10+LPS group), **p = .0079 (WT+rIL‐10+LPS group vs. IL‐10 −/−+rIL‐10+LPS group), ***p = .0001, ****p < .0001. Lymphocyte, ****p < .0001. (b, c) Production of cytokines IFN‐γ, IL‐6, G‐CSF and CXCL1/KC in Balf and serum was assessed via ELISA kits. n = 6 biologically independent samples. (b) IFN‐γ, *p = .0216 (WT+Con group vs. WT+LPS group), *p = .0333 (WT+LPS group vs. WT+rIL‐10+LPS group), ***p = .0004, ****p < .0001. IL‐6, **p = .0011 (WT+Con group vs. WT+LPS group), **p = .0064, ***p = .0002 (IL‐10 −/−+LPS group vs. IL‐10 −/−+rIL‐10+LPS group), ****p < .0001. G‐CSF, *p = .0445, **p = .0012, ***p = .0002, ****p < .0001. CXCL1/KC, *p = .0127 (WT+Con group vs. WT+LPS group), *p = .0447 (WT+LPS group vs. WT+rIL‐10+LPS group), ****p < .0001. (c) IFN‐γ, **p = .0039, ****p < .0001. IL‐6, **p = .0028, ***p = .0005 (IL‐10 −/−+LPS group vs. IL‐10 −/−+rIL‐10+LPS group), ***p = .0002 (WT+LPS group vs. IL‐10 −/−+LPS group), ****p < .0001. G‐CSF, **p = .0088, ****p < .0001. CXCL1/KC, **p = .0034 (WT+Con group vs. WT+LPS group), **p = .0013 (IL‐10 −/−+LPS group vs. IL‐10 −/−+rIL‐10+LPS group), ****p < .0001. (d) Immunoblotting and its quantitative analysis indicating the effect of IL‐10 on the NLRP3/Caspase‐1 activation for lung inflammation. n = 6 biologically independent samples. NLRP3, **p = .0099, ***p = .0009, ****p < .0001. Caspase‐1 p10, ***p = .0003, **p = .0042, ****p < .0001. (e) Representative images of H&E‐stained lung tissue sections of WT or IL‐10 −/− mice after LPS stimulation for 24 h with or without rIL‐10 treatment. Scale bars in the upper panel, 200 µm; scale bars in the lower panel, 50 µm. Lung damage was determined by 5 pathophysiological features to obtain the total injury score. n = 6 biologically independent samples. ****p < .0001. (f) After LPS stimulation (100 ng/mL) for 6 h with or without rIL‐10 pretreatment, the mRNA expressions of cytokines IL‐1β, and IL‐6 were examined by qRT‐PCR. Data are expressed as fold change. n = 6 biologically independent samples. ****p < .0001. (g) Immunoblotting and its quantitative analysis showing the effect of IL‐10 on the NLRP3/Caspase‐1 activation for macrophage inflammation after 24 h of LPS stimulation (100 ng/mL). n = 3 biologically independent samples. NLRP3, **p = .0077 (WT+Con group vs. WT+LPS group), **p = .0026 (IL‐10 −/−+Con group vs. IL‐10 −/−+LPS group). Caspase‐1 p10, **p = .0046 (IL‐10 −/−+Con group vs. IL‐10 −/−+LPS group), **p = .0036 (WT+LPS group vs. IL‐10 −/−+LPS group), *p = .0344 (IL‐10 −/−+LPS group vs. IL‐10 −/−+rIL‐10+LPS group), *p = .0419 (WT+rIL‐10+LPS group vs. IL‐10 −/−+rIL‐10+LPS group). (h, i) Microplate reader assay exhibiting the effect of IL‐10 expression on the production of mitochondrial (h) and intracellular ROS (i) induced by LPS (100 ng/mL) in BMDMs. n = 6 biologically independent samples. (h) *p = .0122, ***p = .0005, ****p < .0001. (i) **p = .0044, ****p < .0001. (j) Confocal microscopy images showing the mitochondrial mass of BMDMs from each group using MitoTracker probe. Scale bars, 20 µm. (k) Immunoblotting and its quantitative analysis indicating the effect of IL‐10 on the expression of OPA1, MFN2, DRP1 and FIS1 for mitochondrial dynamics in BMDMs. n = 3 biologically independent samples. OPA1, *p = .0145 (WT+Con group vs. WT+LPS group), *p = .015 (IL‐10 −/−+Con group vs. IL‐10 −/−+LPS group), *p = .012. MFN2, **p = .0098, ***p = .0003, *p = .0159 (IL‐10 −/−+Con group vs. IL‐10 −/−+LPS group), *p = .0238 (IL‐10 −/−+LPS group vs. IL‐10 −/−+rIL‐10+LPS group). DRP1, **p = .0082, *p = .0358 (WT+LPS group vs. WT+rIL‐10+LPS group), *p = .0043 (IL‐10 −/−+LPS group vs. IL‐10 −/−+rIL‐10+LPS group), *p = .0157 (WT+LPS group vs. IL‐10 −/−+LPS group), *p = .0131 (WT +rIL‐10+LPS group vs. IL‐10 −/−+rIL‐10+LPS group), ****p < .0001. FIS1, ****p < .0001, **p = .0024, *p = .0332. Data are presented as mean ± SEM and analysed with a 95% confidence interval. p Values were calculated using one‐way ANOVA followed by Bonferroni's post hoc test.

Be the first to write a review!

Citations:

(17)

Figures:

$153.00 Inquire

from
Cell Signaling Technology for
FIS1 (E3K9O) Rabbit mAb

The FIS1 (E3K9O) Rabbit mAb Antibody from Cell Signaling Technology is a Rabbit Monoclonal antibody to Fis1. This antibody recognizes Homo Sapiens, Human, Mouse, and Rat antigen. The FIS1 (E3K9O) Rabbit mAb Antibody has been shown to work in the following applications: Precipitation, Immunocytochemistry, Immunofluorescence, Immunoprecipitation, and Western Blot.

Product Specs
ItemFIS1 (E3K9O) Rabbit mAb
CompanyCell Signaling Technology
Price $153.00 Inquire
Catalog Number32525T
Quantity20 µl
ApplicationsW, IP, IF-F, IF-IC
ReactivityH, M, R
HostRabbit
TargetFIS1
ClonalityMonoclonal
NCBI Full Gene Namefission, mitochondrial 1
NCBI Gene AliasesCGI-135, TTC11

Add to Compare List

Cell Signaling Technology

3 Trask Lane

Danvers, Massachusetts 01923

United States

Phone: 877-616-CELL
Phone: 978-867-2388
Fax: 866-432-6112
Fax: 978-867-2488

Company Profile

Website: http://www.cellsignal.com/

Website: Technical Support

(1) Protective role of fatty acid oxidation against epithelial barrier dysfunction in allergic asthmaRedox ReportDecember 31, 2026Muyun Wang, Yanan He, Haiyang Hu, Di Wu, Ximing Liao, Jing Gao, Shaoyong Gao, Huiming Yin, Kian Fan Chung, Qiang Li, et al.anti-CPT1A (Abcam, UK, ab234111), anti-DRP1 (Cell Signaling Technology, CST, USA, 8570), anti-FIS1 (CST, 32525), anti-OPA1 (CST, 80471), anti-MFN2 (CST, 9482), anti-NLRP3 (CST, 15101), Anti-Caspase-1 (Abcam, ab179515),

(2) Nanoparticle-Loaded Injectable Hydrogel Alleviates Titanium Particle-Induced Osteolysis by Disrupting GATA6/DDX3X-Mediated Macrophage InflammationBiomaterials ResearchApril 16, 2026Sipeng Lin, Taihe Liu, Qi Zhu, Zhuji Ouyang, Yifan Yu, Haopeng Sun, Changchuan Li, Shixun Li, Chenhao Pan, Wing Cheuk Ko, et al.(Rabbit, 29047, Cell Signaling Technology), DRP1 (Rabbit, 8570, Cell Signaling Technology), FIS1 (Rabbit, 32525, Cell Signaling Technology), and GATA6 (Rabbit, 5851, Cell Signaling Technology). RNA-seq Total RNA

(3) A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injuryCell Rep MedMarch 17, 2026Zhaoyi Che, Zhihui Luo, Dong Xiao, Fashu Ma, Haoxiong Zhou, Yali Song, Shanshan Guo, Yuan Yuan, Hao Wang, Ching-Pong Mak, et al.antibody,Cell Signaling Technology,Cat#8570; RRID:AB_10950498 Anti-FIS1 antibody,Cell Signaling Technology,Cat#32525; RRID:AB_2927422 Anti-OPA1 antibody,Cell Signaling Technology,Cat#80471; RRID:AB_2734117 Anti-Bcl-2

(4) Cys340Ser Mutation Abolishing S-Nitrosylation Drives GRK2 Mitochondrial Localization and DysfunctionCellsMarch 4, 2026Gizem Kayki Mutlu, Stephanie M. Kereliuk, Maya Hoteit, J. Kurt Chuprun, Umur Mendes, Yusuf Olgar, Walter J. KochSigma Aldrich, St. Louis, MO, USA), Drp1 (8570; Cell Signaling Technology, Danvers, MA, USA), Fis1 (32525; Cell Signaling Technology, Danvers, MA, USA), Mfn1 (14739; Cell Signaling Technology, Danvers, MA,

(5) Modeling the cell biology of PEX11β deficiency during human neurogenesisbioRxivFebruary 19, 2026C Bodnya, R P Theart, V Gama(1:200),Cell Signaling Technologies,Cat #84580 Rabbit anti-FIS1 (1:200),Cell Signaling Technologies,Cat #32525 Rabbit anti-ACBD5 (1:200),Sigma-Aldrich,Cat #HPA012145-100uL Mouse anti-Nestin (1:100),Stem Cell Technologies,Cat

(6) Metformin Attenuates Osteoarthritis Progression by Modulating Mitochondrial Dynamics via Activation of the AMPK/Drp1 PathwayJournal of Inflammation ResearchFebruary 2, 2026Yaji Yang, Haotian Zhou, Jianye Yang, Feilong Li, Qianshui Hu, Ying Jia, Wei Huang, Leilei Qin, Yu Zhouanti-GAPDH (CST, #97166); anti-DRP1 (CST, #8570); anti-phospho-DRP1 (CST, # 20990); anti-Fis1 (CST, #32525); anti-P62 (CST, #39749); anti-LC3B (CST, #2775); anti-PINK1 (CST, #6946); anti-Parkin (CST, #2132);

(7) Metformin Attenuates Osteoarthritis Progression by Modulating Mitochondrial Dynamics via Activation of the AMPK/Drp1 PathwayJ Inflamm ResFebruary 2, 2026Yaji Yang, Haotian Zhou, Jianye Yang, Feilong Li, Qianshui Hu, Ying Jia, Wei Huang, Leilei Qin, Yu Zhouanti-GAPDH (CST, #97166); anti-DRP1 (CST, #8570); anti-phospho-DRP1 (CST, # 20990); anti-Fis1 (CST, #32525); anti-P62 (CST, #39749); anti-LC3B (CST, #2775); anti-PINK1 (CST, #6946); anti-Parkin (CST, #2132);

(8) Therapeutic Effects of Noninvasive Electrical Stimulation in Combination Transplantation of Human Adipose‐Derived Stem Cells‐Derived Dopaminergic Neuron on the Monkey Model of Parkinson's DiseaseMedComm (2020)February 1, 2026Chunhui Huang, Shane Gao, Xiao Zheng, Xichen Song, Jiaxi Wu, Kai Liao, Jiawei Li, Yingqi Lin, Caijuan Li, Yaqun Lu, et al.60004‐1‐Ig), MNF1 (abcam; ab126575), MNF2 (CST; 9482S), OPA1 (CST; 80471S), DRP1 (abcam; ab56788), Fis1 (CST; 32525S), NeuN (abcam; ab177487), PSD95 (CST; 2507S), synapsin‐1 (CST; 5297S), synaptophysin (CST; 25056S),

(9) Rg1-R1 attenuates cardiac ischemia/reperfusion-induced endothelial cell injury through activating the ULK1/PGAM5-FUNDC1-mitophagy pathwayJournal of Ginseng ResearchDecember 31, 2025Xiayinan Song, Jinlan Deng, Danyang Wang, Zhenzhen Zheng, Chao Li, Jie LiAbcam, USA), e-NOS(#32027, CST, USA), Mitofusin-2 (#9482, CST, USA), OPA1 (#80471, CST, USA), Fis1 (#32525, CST, USA), p-DRP1(#4494, CST, USA), DRP1(#8570, CST, USA), FUNDC1(#49240, CST, USA), P-FUNDC1(PA5-114576,

(10) PPA2 activates MTFP1-DNM1L fission signaling to govern mitochondrial proliferation and mitophagyAutophagySeptember 9, 2025Soumya Ranjan Mishra, Priyadarshini Mishra, Kewal Kumar Mahapatra, Bishnu Prasad Behera, Gajanan Kendre, Moureq Rashed Alotaibi, Vijay Pandey, Birija Sankar Patro, Daniel J. Klionsky, Sujit Kumar BhutiaCOX4/COXIV (4844S; 1: 6000 WB), COX4/COXIV (4850; 1:1000 IF), p-DNM1L/DRP1 Ser616 (3455S; 1:1000 WB), FIS1 (32525; 1:1000 WB), LAMP1 (9091, 1:500 IF) and MFF (84580; 1:1000 WB) were purchased from Cell Signaling Technology.

(11) Astaxanthin mitigates cardiac toxicity induced via doxorubicin by alleviating mitochondrial fission and autophagy in ratsScientific ReportsSeptember 1, 2025Yongjing He, Dan Wu, Qianqian Wu, Sisi Huang, Yuansheng Zhan, Jiaqiang Deng, Jing yu Chen, Lu xie, Junhui Zheng27733-1-AP), Beclin-1(1:1000, Cell Signaling Technology, #3495) and Fis-1(1:1000, Cell Signaling Technology, #32525). After washing the membrane three times with TBST for ten minutes each time, it was incubated with

(12) The loss of OPA1 accelerates intervertebral disc degeneration and osteoarthritis in aged miceNat CommunJuly 1, 2025Vedavathi Madhu, Miriam Hernandaz-Meadows, Ashley Coleman, Kimheak Sao, Kameron Inguito, Owen Haslam, Paige K. Boneski, Hiromi Sesaki, Ruteja A. Barve, John A. Collins, et al.(12741), LAMP1 (9091), SQSTM1/p62 (5114), CHOP (78063), Beclin1 (3738), MFF (84580), MFN2 (9482), FIS1 (32525), Ub (3933), pUb (62802), GAPDH (5174) (Cell Signaling), DRP1 (611113), OPA1 (612607) (BD Biosciences,

(13) Therapeutic Potential of STE20-Type Kinase STK25 Inhibition for the Prevention and Treatment of Metabolically Induced Hepatocellular CarcinomaCellular and Molecular Gastroenterology and HepatologyFebruary 28, 2025Ying Xia, Mara Caputo, Emma Andersson, Bernice Asiedu, Jingjing Zhang, Wei Hou, Manoj Amrutkar, Emmelie Cansby, Nadia Gul, Anne Gemmink, et al.(#9482),1:1000,Cell Signaling Technology ,anti-DRP1 (#8570),1:1000,Cell Signaling Technology ,anti-FIS1 (#32525),1:1000,Cell Signaling Technology ,anti-MST4 (#3822)anti-GAPDH (sc-47724)anti-vinculin (sc-25336),1:10001:10001:500,Cell Signaling

(14) Protective effects of Notoginsenoside R2 on reducing lipid accumulation and mitochondrial dysfunction in diabetic nephropathy through regulation of c-SrcChin MedJanuary 15, 2025Xieyi Guo, Liu Yang, Xiaoning An, Maofang Hu, Yilan Shen, Niansong Wang, Youhua Xu, Dingkun GuiSrc (2123), p-JNK (9252), JNK (9251), p-STAT1 (7649), STAT1 (9172), Drp1 (8750), Mfn2 (9482), Fis1 (32525), Bcl-2 (3498), cleaved-caspase-3 (9664) were from CST (USA). CD36 (ab252922) was obtained from Abcam

(15) CPT1A‐IL‐10‐mediated macrophage metabolic and phenotypic alterations ameliorate acute lung injuryClinical and Translational MedicineAugust 1, 2024Muyun Wang, Di Wu, Ximing Liao, Haiyang Hu, Jing Gao, Linlin Meng, Feilong Wang, Wujian Xu, Shaoyong Gao, Jing Hua, et al.including anti‐CPT1A (Abcam, ab234111, UK), DRP1 (Cell Signaling Technology, CST, 8570, USA), FIS1 (CST, 32525), OPA1 (CST, 80471), MFN2 (CST, 9482), NLRP3 (CST, 15101), ARG1 (CST, 93668), iNOS (CST, 13120), Caspase‐1

(16) The loss of OPA1 accelerates intervertebral disc degeneration and osteoarthritis in aged miceResearch SquareFebruary 21, 2024Makarand Risbud, Vedavathi Madhu, Miriam Hernandez-Meadows, Ashley Coleman, Kimheak Sao, Kameron Inguito, Owen Haslam, Paige Boneski, Hiromi Sesaki, John Collinsanti-p62 (5114), anti-CHOP (78063), anit-Beclin1 (3738), anti-MFF (84580), anti-MFN2 (9482), anti-FIS1 (32525), anti-Ub (#), pUb (62802), anti-GAPDH (5174) (Cell Signaling), anti-DRP1 (611113), anti-OPA1 (612607)

(17) Novel Relationship between Mitofusin 2-Mediated Mitochondrial Hyperfusion, Metabolic Remodeling, and Glycolysis in Pulmonary Arterial Endothelial CellsInternational journal of molecular sciencesDecember 15, 2023Yegambaram M, Sun X, Flores AG, Lu Q, Soto J, Richards J, Aggarwal S, Wang T, Gu H, Fineman JR, et al.antibody (#5391S, Cell Signaling Technologies, Danvers, MA, USA), a primary monoclonal Fis1 antibody (#32525S, Cell Signaling Technologies, Danvers, MA, USA), a primary monoclonal HIF-1α antibody (#NB100-105SS,

Be the First to Write a Review!

Clinical and Translational Medicine

Clinical and Translational Medicine

Chin Med

International journal of molecular sciences

Clinical and Translational Medicine

FIS1 (E3K9O) Rabbit mAb from Cell Signaling Technology

Cell Signaling Technology

Citations (17)

Reviews

FIS1 (E3K9O) Rabbit mAb from Cell Signaling Technology

About Biocompare

Advertise with Us

Specialized Search Tools

Site Map