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mouse monoclonal anti c fos e 8  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology mouse monoclonal anti c fos e 8
    Mouse Monoclonal Anti C Fos E 8, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 4523 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/c+fos/c-Fos+Antibody/pmc13045675-3-0-7
    Average 96 stars, based on 4523 article reviews
    mouse monoclonal anti c fos e 8 - by Bioz Stars, 2026-09
    96/100 stars

    Images

    Related Articles

    Marker:

    Article Title: Designed bone-targeting ROS-responsive nanoplatform for precision glycolysis inhibition in postmenopausal osteoporosis
    Article Snippet: Cell culture supplies, including α-MEM and fetal bovine serum (FBS), were sourced from Thermo Fisher Scientific in Carlsbad, United States. .. Antibodies against osteoclast marker proteins, such as c-Fos, CTSK, integrin β3, and NFATc1, were procured from Santa Cruz (San Jose, United States). .. Moreover, antibodies targeting p-P38, P38, p-JNK, JNK, p-ERK, ERK, p-P65, P65, and IκB-α were sourced from Cell Signaling Technology, Danvers, United States.

    Western Blot:

    Article Title: An alkaline nanosized platelet vesicle-based hydrogel for the treatment of osteoporotic bone defects
    Article Snippet: .. Western blotting was used to evaluate the protein expression of NFATc1 (sc-7294, Santa Cruz), c-Fos (sc-166940, Santa Cruz), CTSK (11239-1-AP, ProteinTech), and β-actin (20536-1-AP, ProteinTech). ..

    Expressing:

    Article Title: An alkaline nanosized platelet vesicle-based hydrogel for the treatment of osteoporotic bone defects
    Article Snippet: .. Western blotting was used to evaluate the protein expression of NFATc1 (sc-7294, Santa Cruz), c-Fos (sc-166940, Santa Cruz), CTSK (11239-1-AP, ProteinTech), and β-actin (20536-1-AP, ProteinTech). ..

    Incubation:

    Article Title: Standing strong: Effects of social dominance on neural activity and defeat-induced social avoidance in female Syrian hamsters.
    Article Snippet: Social dominance modulates stress vulnerability, yet the neural mechanisms by which dominance status alters responses to stress in females remain poorly understood.. This study aimed to determine whether activation of neurons in the posterior medial amygdala (MeP) and ventral medial prefrontal cortex (vmPFC) was associated with reduced stress vulnerability in dominant female Syrian hamsters.. We created dominance relationships in hamsters, exposed animals to social defeat stress, tested animals for stress-induced social avoidant responses, and collected tissue for c-Fos immunohistochemistry.

    Article Title: Ensembles and engrams in mouse cortical and sub-thalamic brain regions supporting context and memory recall.
    Article Snippet: Associative learning supports learning about outcomes associated with contexts and cues.. During learning, cellular ensembles that become active can be incorporated into memory engrams and later reactivated to support recall.. Studies exploring engram formation and reactivation have primarily used contextual conditioning in mice and made little distinction between ensembles supporting contextual information versus cue-associated learning and recall.

    other:

    Article Title: Therapeutic potency and the related mechanism of deinoxanthin in experimental animal and cell models of periodontitis.
    Article Snippet: Cathepsin K (sc-4835), β-actin (sc-47778), c-Fos (sc-166940), matrix metalloproteinase-9 (MMP-9; sc-393859), and nuclear factor of activated Tcells, cytoplasmic 1 (NFATc1; sc-7294) antibodies were provided by Santa Cruz Biotechnology (Santa Cruz, CA, USA).

    Article Title: Tonsil‑derived mesenchymal stem cell‑derived extracellular vesicles suppress MAPK‑NF‑κB signaling and restore osteogenic differentiation in LPS‑stimulated periodontal ligament fibroblasts.
    Article Snippet: Primary antibodies against β‐actin, p65, c‐Jun, and c‐Fos (Santa Cruz Biotechnology, Inc.), as well as phosphorylated or total extracellular signal‐regulated kinase (ERK) and c‐Jun N‐terminal kinase (JNK) (Cell Signaling Technology) were used at a dilution of 1:1,000.

    Bioprocessing:

    Article Title: Sibelium exerts anti-migraine effects by remodeling the gut microbiota and regulating metabolic and immune pathways of the brain-gut axis.
    Article Snippet: Background/objectives: Migraine is a highly disabling neurological disorder closely associated with the brain-gut axis.. The mechanism of action of sibelium (flunarizine), a commonly used prophylactic medication, is unclear but may act through modulation of the gut microbiota.. Based on the “brain-gut-microbiota axis” theory, the effects of sibelium on gut microbiota and the underlying mechanism for migraine prevention were investigated.



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    AP-1 <t>(c-FOS</t> and c-JUN) is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by <t>CD.</t> <t>β-Actin</t> served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.
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    AP-1 <t>(c-FOS</t> and c-JUN) is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by <t>CD.</t> <t>β-Actin</t> served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.
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    AP-1 <t>(c-FOS</t> and c-JUN) is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by <t>CD.</t> <t>β-Actin</t> served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.
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    AP-1 <t>(c-FOS</t> and c-JUN) is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by <t>CD.</t> <t>β-Actin</t> served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.
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    AP-1 <t>(c-FOS</t> and c-JUN) is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by <t>CD.</t> <t>β-Actin</t> served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.
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    Image Search Results


    AP-1 (c-FOS and c-JUN) is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by CD. β-Actin served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.

    Journal: Life Medicine

    Article Title: HDAC8-selective inhibitor PCI-34051 protects against aortic dissection by attenuating ferroptosis of vascular smooth muscle cells

    doi: 10.1093/lifemedi/lnag013

    Figure Lengend Snippet: AP-1 (c-FOS and c-JUN) is a key regulator of PCI-34051 in the regulation of HASMC ferroptosis. (A) Volcano plot displaying the gene expression distribution and differentially expressed genes among the DMSO and PCI-34051 groups after treatment with CD. (B) Gene Ontology (GO) enrichment analysis showed that biological processes and cellular components were associated with these differentially expressed genes. (C, D) Western-blot analysis and quantification showing the protein levels of c-FOS and c-JUN in HASMCs after treatment with DMSO and PCI-34051 under the ferroptosis models induced by CD. β-Actin served as a loading control ( n = 4 per group). (E, F) Co-immunoprecipitation results showed that HDAC8 interacted with c-JUN in HASMCs. (G) Results of GST pull-down demonstrated a direct interaction between HDAC8 and c-JUN in HASMCs. Values are means ± SD; *** P < 0.001. BP, biological process. CC, cellular component. MF, molecular function.

    Article Snippet: The antibodies applied in this study were: β-Actin (AC026, ABclonal), FSP1 (20886-1-AP, Proteintech), GPX4 (ab125066, Abcam), c-JUN (T55290F, ABmart), c-FOS (T56596F, ABmart), Flag (F1804, Sigma-Aldrich), HDAC8 (17548-1-AP, Proteintech), SLC7A11 (26864-1-AP, Proteintech), 4-HNE (MAB3249-SP, Bio-techne), CD86 (13395-1-AP, Proteintech), α-SMA (ab7817, Abcam), α-SMA (GTX100034, Genetex), GST (AE001, Abclonal).

    Techniques: Gene Expression, Western Blot, Control, Immunoprecipitation

    AP-1 (c-FOS and c-JUN) eliminated the effects of PCI-34051 on HASMC ferroptosis. All HASMCs were infected with lenti-Flag and lenti-c-FOS + lenti-c-JUN, and then these HASMCs were used for subsequent experiments. (A, B) The protein level of AP-1 (c-JUN and c-FOS) was detected by Western blot in HASMCs infected with lenti-Flag and lenti-c-JUN + lenti-c-FOS ( n = 4 per group). (C, D) The CCK8 assay showing the relative viability of HASMCs treated with DMSO and PCI-34051 after CD (C) and IKE (D) stimulation for the indicated time ( n = 5 per group). (E, F) Flow cytometry with propidium iodide (PI) staining displaying the percentage of PI-positive cells of HASMCs after treatment as described above ( n = 4 per group). (G, H) The LDH assay indicating the relative cell damage rate of HASMCs treated with described above ( n = 5 per group). (I–L) The ratio of oxidized BODIPY-C11/non-oxidized BODIPY-C11 fluorescence revealing the level of ROS of HASMCs treated with described above ( n = 4 per group). (M–P). 4-HNE immunofluorescence staining and quantitative analysis exhibiting the content of 4-HNE in HASMCs after treatment as described above ( n = 4 per group). (Q–T) Western-blot analysis and quantification performed to assess the protein levels of GPX4, FSP1, and SLC7A11 in AP-1 overexpressed HASMCs after DMSO and PCI-34051 treatment along with CD or IKE induction. β-Actin served as a loading control ( n = 4 per group). Values are means ± SD; *** P < 0.001, ** P < 0.01, * P < 0.05.

    Journal: Life Medicine

    Article Title: HDAC8-selective inhibitor PCI-34051 protects against aortic dissection by attenuating ferroptosis of vascular smooth muscle cells

    doi: 10.1093/lifemedi/lnag013

    Figure Lengend Snippet: AP-1 (c-FOS and c-JUN) eliminated the effects of PCI-34051 on HASMC ferroptosis. All HASMCs were infected with lenti-Flag and lenti-c-FOS + lenti-c-JUN, and then these HASMCs were used for subsequent experiments. (A, B) The protein level of AP-1 (c-JUN and c-FOS) was detected by Western blot in HASMCs infected with lenti-Flag and lenti-c-JUN + lenti-c-FOS ( n = 4 per group). (C, D) The CCK8 assay showing the relative viability of HASMCs treated with DMSO and PCI-34051 after CD (C) and IKE (D) stimulation for the indicated time ( n = 5 per group). (E, F) Flow cytometry with propidium iodide (PI) staining displaying the percentage of PI-positive cells of HASMCs after treatment as described above ( n = 4 per group). (G, H) The LDH assay indicating the relative cell damage rate of HASMCs treated with described above ( n = 5 per group). (I–L) The ratio of oxidized BODIPY-C11/non-oxidized BODIPY-C11 fluorescence revealing the level of ROS of HASMCs treated with described above ( n = 4 per group). (M–P). 4-HNE immunofluorescence staining and quantitative analysis exhibiting the content of 4-HNE in HASMCs after treatment as described above ( n = 4 per group). (Q–T) Western-blot analysis and quantification performed to assess the protein levels of GPX4, FSP1, and SLC7A11 in AP-1 overexpressed HASMCs after DMSO and PCI-34051 treatment along with CD or IKE induction. β-Actin served as a loading control ( n = 4 per group). Values are means ± SD; *** P < 0.001, ** P < 0.01, * P < 0.05.

    Article Snippet: The antibodies applied in this study were: β-Actin (AC026, ABclonal), FSP1 (20886-1-AP, Proteintech), GPX4 (ab125066, Abcam), c-JUN (T55290F, ABmart), c-FOS (T56596F, ABmart), Flag (F1804, Sigma-Aldrich), HDAC8 (17548-1-AP, Proteintech), SLC7A11 (26864-1-AP, Proteintech), 4-HNE (MAB3249-SP, Bio-techne), CD86 (13395-1-AP, Proteintech), α-SMA (ab7817, Abcam), α-SMA (GTX100034, Genetex), GST (AE001, Abclonal).

    Techniques: Infection, Western Blot, CCK-8 Assay, Flow Cytometry, Staining, Lactate Dehydrogenase Assay, Fluorescence, Immunofluorescence, Control

    The working model of PCI-34051 regulating HASMC ferroptosis and aortic dissection in mice. PCI-34051 inhibits the ferroptosis of HASMC by affecting the interaction between HDAC8 and AP-1 (c-FOS and c-JUN) and further suppresses the occurrence and development of BAPN-induced aortic dissection in mice. (This figure is created with Biorender).

    Journal: Life Medicine

    Article Title: HDAC8-selective inhibitor PCI-34051 protects against aortic dissection by attenuating ferroptosis of vascular smooth muscle cells

    doi: 10.1093/lifemedi/lnag013

    Figure Lengend Snippet: The working model of PCI-34051 regulating HASMC ferroptosis and aortic dissection in mice. PCI-34051 inhibits the ferroptosis of HASMC by affecting the interaction between HDAC8 and AP-1 (c-FOS and c-JUN) and further suppresses the occurrence and development of BAPN-induced aortic dissection in mice. (This figure is created with Biorender).

    Article Snippet: The antibodies applied in this study were: β-Actin (AC026, ABclonal), FSP1 (20886-1-AP, Proteintech), GPX4 (ab125066, Abcam), c-JUN (T55290F, ABmart), c-FOS (T56596F, ABmart), Flag (F1804, Sigma-Aldrich), HDAC8 (17548-1-AP, Proteintech), SLC7A11 (26864-1-AP, Proteintech), 4-HNE (MAB3249-SP, Bio-techne), CD86 (13395-1-AP, Proteintech), α-SMA (ab7817, Abcam), α-SMA (GTX100034, Genetex), GST (AE001, Abclonal).

    Techniques: Dissection