mouse tnfr2 (Hycult Biotech)
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Hycult Biotech
mouse tnfr2
Mouse Tnfr2, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mouse tnfr2/product/Hycult Biotech
Average 90 stars, based on 1 article reviews
Mouse Tnfr2, supplied by Hycult Biotech, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mouse tnfr2/product/Hycult Biotech
Average 90 stars, based on 1 article reviews
mouse tnfr2 - by Bioz Stars,
2025-04
90/100 stars
Images
1) Product Images from "Essential protective role of tumor necrosis factor receptor 2 in neurodegeneration"
Article Title: Essential protective role of tumor necrosis factor receptor 2 in neurodegeneration
Journal: Proceedings of the National Academy of Sciences of the United States of America
doi: 10.1073/pnas.1605195113
Figure Legend Snippet: Genetic engineering and bioactivity of EHD2–scTNFR2. (A) Schematic representation of EHD2–scTNFR2. (B) Coomassie staining and immunoblot of EHD2–scTNFR2 under reducing (column 1) and nonreducing (column 2) conditions. (C) HPLC-SEC analysis of EHD2–scTNFR2 using a BioSep-Sec-2000 column. Peak positions of relevant standard proteins are indicated. (D and E) Binding of soluble huTNF (□) and membrane-TNF mimetic EHD2–scTNFR2 (●) to huTNFR1 (huTNFR1–Fc) or huTNFR2 (Etanercept; huTNFR2–Fc) was determined by ELISA (n = 3; ±SEM). (F) L929 cells were cultivated with titrations of recombinant human TNF (huTNF) or EHD2–scTNFR2. Cell viability was determined by crystal violet staining (n = 4; mean ± SEM). (G) Kym-1 cells were stimulated with (open symbols) or without (closed symbol) the TNFR2 cross-linking mAb 80M2 for 30 min at 37 °C. Then titrations of scTNFR2 (squares) or EHD2–scTNFR2 (circles) were added and cells were incubated for 24 h. Cell viability was determined by crystal violet staining (n = 4–6; mean ± SEM).
Techniques Used: Staining, Western Blot, Binding Assay, Enzyme-linked Immunosorbent Assay, Recombinant, Incubation
Figure Legend Snippet: Southern blot analysis of mouse tissue. DNA from lung, heart, liver, brain, thymus, kidney, and skin tissue from homozygous hu/mTNFR1-k/i (A). (B) hu/mTNFR2-k/i mice were digested by BamHI, blotted on nylon membrane, and probed with the endogenous probes enP. Genomic DNA from tail biopsies of wild-type mice was used as a control. The DNA size marker phage Lambda DNA/StyI marker (Bioron) was used to identify size of products. In all samples, the neo cassette is removed as evident by the 5.9-kb (A; hu/mTNFR1-k/i) or 8.2-kb (B; hu/TNFR2-k/i) product.
Techniques Used: Southern Blot, Marker, Lambda DNA Preparation
Figure Legend Snippet: Expression of transgenic hu/mTNFR1-k/i and hu/mTNFR2-k/i in homozygous mice. Splenocytes or thymocytes were isolated from C57BL/6J wild-type (A and B), hu/mTNFR1-k/i (A), or hu/mTNFR2-k/i (B) mice. Then mouse TNFR1 (HP8002) and human TNFR1 (HP9002) (A) or mouse TNFR2 (HP8003) and human TNFR2 (HP9003) (B) expression was analyzed by flow cytometry using subgates for CD45R+ B cells, CD68+ macrophages (splenocytes), and CD8+ thymocytes. Gray histograms show the isotype controls; black lines indicate signals measured for TNFR1 or TNFR2 expression. Data are presented as normalized to unit area.
Techniques Used: Expressing, Transgenic Assay, Isolation, Flow Cytometry
Figure Legend Snippet: Expression of transgenic hu/mTNFR1-k/i and hu/mTNFR2-k/i in primary cells isolated from homozygous mice. Primary MEFs were isolated from wild-type (A and B), hu/mTNFR1-k/i (A), or hu/mTNFR2-k/i (B) C57BL/6 mice. Expression of mouse TNFR1 (HP8002) and human TNFR1 (HP9002) (A) or mouse TNFR2 (HP8003) and human TNFR2 (HP9003) (B) was analyzed by flow cytometry. Data are presented as normalized to unit area. (C and D) Brain tissue isolated from wild-type (C and D), hu/mTNFR1-k/I (C), or hu/mTNFR2-k/i (D) C57BL/6 mice. Tissue was lyzed and expression of huTNFR1 (wild-type, hu/mTNFR1-k/i, H398) or huTNFR2 (wild-type, hu/mTNFR2-k/i, MR2-1) was analyzed by Western blot.
Techniques Used: Expressing, Transgenic Assay, Isolation, Flow Cytometry, Western Blot
Figure Legend Snippet: Body weight changes after treatment in both mouse lines. (A) EHD2–scTNFR2 significantly prevented the reduction of body weight induced by NMDA injection into the NBM in hu/mTNFR2-k/i mice at 2 and 4 d after injection. (B) ATROSAB prevented the significant reduction of body weight induced by NMDA injection into the NBM in hu/mTNFR1-k/i mice at 1 d after injection, but this was not statistically significant. (C) Body weight effects of the TNFR2 antagonistic antibody MAB426, when administered together with NMDA alone, or NMDA and ATROSAB together.
Techniques Used: Injection
Figure Legend Snippet: ATROSAB is neuroprotective via enhanced TNFR2 signaling. (A) Primary neurons, isolated from hu/mTNFR1-k/i mice, were stimulated with or without ATROSAB (100 µg/mL) for 30 min followed by addition of wild-type EHD2-sc–mTNF (10 ng/mL). Then cells were incubated for 24 h and lyzed, and phosphorylation of PKB/Akt was quantified by Western blot (n = 4, ±SEM). (B) Primary neurons, isolated from hu/mTNFR1-k/i mice, were stimulated with or without ATROSAB (100 µg/mL) for 30 min followed by addition of non–TNFR-selective EHD2-sc–mTNF or mouse TNFR2-selective EHD2-sc–mTNFR2. After 24 h, glutamate (5 µM) was added and cells were incubated for an additional hour. Then medium was exchanged to remove glutamate and cells were incubated for 23 h. Cell viability was determined by MTT assay. Data are shown as percentage of MTT signal of untreated control cells (n = 3; ±SEM). Representative images show (C) ChAT-positive cholinergic innervations in the somatosensory cortex or (E) CD11B-positive activated macrophage/microglia in magnocellular nucleus basalis. NMDA injected into the NBM induced an extensive cholinergic fiber loss in the layer V of somatosensory cortex and a massive volume of macrophage/microglial activation compared with the control group. However, ATROSAB treatment attenuated fiber loss and significantly reduced macrophage/microglial activation induced by NMDA. ATROSAB neuroprotection against fiber loss was prevented by TNFR2 antagonistic MAB426. However, MAB426 alone did not significantly alter NMDA-induced NBM lesion. Parallel bars indicated the layer V of the somatosensory cortex in which quantitative measurements were performed. (D) Quantification of cholinergic fiber density in layer V of the somatosensory cortex. Fiber density was measured in eight sections per mouse. (F) Quantification of total extent of activated macrophage/microglia around the injections. Macrophage/microglial activation was measured in a series of sections with macrophage/microglial activation. n = 7 mice/group. All data in bar charts represent means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.0001, one-way ANOVA with post hoc comparisons Tukey.
Techniques Used: Isolation, Incubation, Western Blot, MTT Assay, Injection, Activation Assay
Figure Legend Snippet: Mechanism of TNFR1 antagonist ATROSAB and TNFR2 agonist EHD2–scTNFR2-mediated neuroprotection. (A) TNFR1 signaling induces neurodegeneration and inflammation, whereas TNFR2 signaling promotes neuroprotection. (B) ATROSAB, an antagonistic TNFR1-selective antibody, can block TNFR1 signaling, leading to prevention of neurodegeneration and inflammation. More importantly, in the presence of ATROSAB, tmTNF stays free to activate neuroprotective signaling via TNFR2. Our data indicate that, by blocking TNFR1, ATROSAB shifts the endogenous tmTNF signaling toward neuroprotective TNFR2 signaling. Similarly, the TNFR2 agonist EHD2–scTNFR2 can directly activate TNFR2 and thereby induce neuroprotection.
Techniques Used: Blocking Assay