c-Fos Antibody - #AF5354

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产品: c-Fos 抗体
货号: AF5354
描述: Rabbit polyclonal antibody to c-Fos
应用: WB IHC IF/ICC IP
文献验证: WB, IHC, IF/ICC
反应: Human, Mouse, Rat
预测: Pig, Bovine, Horse, Rabbit, Dog
蛋白号: P01100
RRID: AB_2837839

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 50ul RMB¥ 1250 现货
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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, IP, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user. For optimal experimental results, antibody reuse is not recommended.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat
克隆:
Polyclonal
特异性:
c-Fos Antibody detects endogenous levels of total c-Fos.
RRID:
AB_2837839
引用格式: Affinity Biosciences Cat# AF5354, RRID:AB_2837839.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

Activator protein 1; AP 1; C FOS; Cellular oncogene c fos; Cellular oncogene fos; FBJ murine osteosarcoma viral (v fos) oncogene homolog (oncogene FOS); FBJ murine osteosarcoma viral oncogene homolog; FBJ murine osteosarcoma viral v fos oncogene homolog; FBJ Osteosarcoma Virus; FOS; FOS protein; FOS_HUMAN; G0 G1 switch regulatory protein 7; G0/G1 switch regulatory protein 7; G0S7; Oncogene FOS; p55; proto oncogene c Fos; Proto oncogene protein c fos; Proto-oncogene c-Fos; v fos FBJ murine osteosarcoma viral oncogene homolog;

抗原和靶标

免疫原:

A synthesized peptide derived from human c-Fos, corresponding to a region within N-terminal amino acids.

基因/基因ID:
FOS(2353)
描述:
Nuclear phosphoprotein which forms a tight but non-covalently linked complex with the JUN/AP-1 transcription factor. In the heterodimer, FOS and JUN/AP-1 basic regions each seems to interact with symmetrical DNA half sites.

研究领域

· Cellular Processes > Cell growth and death > Apoptosis.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > cAMP signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Endocrine resistance.

· Human Diseases > Substance dependence > Amphetamine addiction.

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Parasitic > Leishmaniasis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Colorectal cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Breast cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Choline metabolism in cancer.   (View pathway)

· Human Diseases > Immune diseases > Rheumatoid arthritis.

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

· Organismal Systems > Immune system > Toll-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Th1 and Th2 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > Th17 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > T cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > B cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Environmental adaptation > Circadian entrainment.

· Organismal Systems > Nervous system > Cholinergic synapse.

· Organismal Systems > Nervous system > Dopaminergic synapse.

· Organismal Systems > Endocrine system > Estrogen signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Prolactin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Oxytocin signaling pathway.

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

文献引用

1). Prolonged anesthesia induces neuroinflammation and complement-mediated microglial synaptic elimination involved in neurocognitive dysfunction and anxiety-like behaviors. BMC Medicine, 2023 (PubMed: 36600274) [IF=7.0]

Application: IF/ICC    Species: Rat    Sample: hippocampal

Fig. 2 Prolonged anesthesia inducing neuroinflammation, upregulating NF-κB inflammatory pathway, downregulating neuronal excitability, and inactivating apoptotic signaling. A, B TNF-α, IL-1β, and IL-6 evidently increased in the cortex (A) and hippocampus (B) after prolonged anesthesia (n = 4 or 5 per group). C Effects of prolonged anesthesia on the morphological changes of neurons in the hippocampus. Scale bar = 20 μm. D Prolonged anesthesia activated NF-κB inflammatory pathway (n = 3 per group). E The number of Phospho-NF-κB P65-colocalized nuclei in the hippocampus (n = 4 per group). Scale bar = 10 μm. F Prolonged anesthesia inhibiting neuronal excitability marker C-fos expression in the hippocampal CA1 region (n = 4 per group). Scale bar = 20 μm. G Exhibiting representative EEG raw traces (upper) and power spectrograms (bottom) for the hippocampus. H Prolonged anesthesia triggered burst suppression in the hippocampus (n = 6 per group). The burst suppression ratio (BSR) was calculated as the percentage of suppression time of each 1 min binary series. I TUNEL staining in brain slices was negative after prolonged anesthesia. Scale bar = 100 μm. J The number of Nissl’s body (n = 4 per group). Scale bar = 20 μm. K Prolonged anesthesia had no effect on apoptotic pathways (n = 3 per group). L, M Quantification of Cleaved caspase-3/caspase-3 (L) and bcl-2/bax (M) levels normalized to β-actin. Data was shown as Mean ± SD, with *P < 0.05 or *P < 0.001; Sevo group vs. control group. Arrows represent positive cells or colocalization
2). Effects and Mechanisms of Rhus chinensis Mill. Fruits on Suppressing RANKL-Induced Osteoclastogenesis by Network Pharmacology and Validation in RAW264.7 Cells. Nutrients, 2022 (PubMed: 35267996) [IF=5.9]

Application: WB    Species:    Sample: RAW264.7 cells

Figure 9.| Effects of the ethanolic extract from the R. chinensis fruits on RANKL-induced osteoclastogenesis on c-Fos and NFATc1 proteins in RAW264.7 cells. (a) Western blot analysis of c-Fos and proteins
3). Dehydromiltirone inhibits osteoclast differentiation in RAW264.7 and bone marrow macrophages by modulating MAPK and NF-κB activity. Frontiers in Pharmacology, 2022 (PubMed: 36210855) [IF=5.6]
4). Protective Effects of ζ-Carotene-like Compounds against Acute UVB-Induced Skin Damage. International journal of molecular sciences, 2023 (PubMed: 37762273) [IF=5.6]

Application: WB    Species: Mouse    Sample:

Figure 7 MAPK/AP-1 signaling pathway. (A) is the representative blots. (B–K) are the ratios of JNK, ERK, P38, Jun, c-FOS, p-JNK, p-ERK, p-P38, p-Jun and p-c-FOS to GAPDH (n = 3, ## p < 0.01 vs. the NCS group and * p < 0.05, ** p < 0.01 vs. the MCS group and ns is no significance).
5). JNK signaling pathway mediates acetaminophen-induced hepatotoxicity accompanied by changes of glutathione S-transferase A1 content and expression. Frontiers in Pharmacology, 2019 (PubMed: 31620005) [IF=5.6]

Application: WB    Species: mouse    Sample: liver

FIGURE 2 | Activation of JNK signaling pathway under different dosages of APAP. (A) Western blot analyses of total tissue lysate for p-JNK, JNK, p-c-Jun, c-Jun,p-c-Fos, c-Fos, and β-actin (loading control).
6). Isoginkgetin Inhibits RANKL-induced Osteoclastogenesis and Alleviates Bone Loss. Biochemical pharmacology, 2025 (PubMed: 39613114) [IF=5.3]
7). Neurobehavioral alternations of the female offspring born to polycystic ovary syndrome model rats administered by Chinese herbal medicine. Chinese Medicine, 2021 (PubMed: 34600579) [IF=5.3]
8). 17β-Trenbolone increases the release of lipocalin 2 via the brain‒liver axis and causes Alzheimer's disease-like symptoms in CSDS-induced mice. MOLECULAR NEUROBIOLOGY, 2025 [IF=5.1]
9). CDC42 Regulates the ERK Pathway to Improve Oxygen‒Glucose Deprivation/Reoxygenation-Induced Neural Oxidative Stress and Apoptosis. Molecular neurobiology, 2025 (PubMed: 40035949) [IF=4.6]
10). Phosphorylation at Ser 727 Increases STAT3 Interaction with PKCε Regulating Neuron–Glia Crosstalk via IL-6-Mediated Hyperalgesia In Vivo and In Vitro. MEDIATORS OF INFLAMMATION, 2022 (PubMed: 35125963) [IF=4.4]

Application: WB    Species: Rat    Sample: spinal cords

Figure 5 Expression of proteins related to activated neurocytes detected by Western blot analysis. (a–i) Protein expression of pSTAT3 (Ser727), IL-6, c-Fos, GFAP, and Iba-1 in the spinal cords of FCA-treated rats significant decreased (P < 0.05) after intrathecal injections of PKCε inhibitor peptide (100 μg/50 μL), APTSTAT3-9R (20 μg/50 μL), and anti-IL-6 antibody (100 ng/50 μL). Values were normalized against GAPDH and are expressed as ratios (%) of control values. Data are shown as means ± SD (n = 4–5). ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001; one-way ANOVA followed by Bonferroni tests.
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