产品: RhoA 抗体
货号: AF6352
描述: Rabbit polyclonal antibody to RhoA
应用: WB IHC IF/ICC
文献验证: WB, IHC, IF/ICC
反应: Human, Mouse, Rat, Monkey
预测: Pig, Bovine, Sheep, Dog
蛋白号: P61586
RRID: AB_2835157

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*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, Monkey
克隆:
Polyclonal
特异性:
RhoA Antibody detects endogenous levels of total RhoA.
RRID:
AB_2835157
引用格式: Affinity Biosciences Cat# AF6352, RRID:AB_2835157.
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

Aplysia ras related homolog 12; ARH12; ARHA; H 12; H12; Oncogene RHO H12; Ras homolog family member A; Ras homolog gene family member A; Rho A; Rho cDNA clone 12; RHO H12; RHO12; RHOA; RHOA_HUMAN; RHOH12; Small GTP binding protein Rho A; Transforming protein Rho A; Transforming protein RhoA;

抗原和靶标

免疫原:

A synthesized peptide derived from human RhoA, corresponding to a region within C-terminal amino acids.

基因/基因ID:
描述:
RhoA is a small G protein of the Rho family. Regulates a signal transduction pathway linking plasma membrane receptors to the assembly of focal adhesions and actin stress fibers.

研究领域

· Cellular Processes > Transport and catabolism > Endocytosis.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Focal adhesion.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Adherens junction.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Tight junction.   (View pathway)

· Cellular Processes > Cell motility > Regulation of actin cytoskeleton.   (View pathway)

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

· Environmental Information Processing > Signal transduction > Rap1 signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > cGMP-PKG signaling pathway.   (View pathway)

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

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

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

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

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

· Environmental Information Processing > Signal transduction > TGF-beta signaling pathway.   (View pathway)

· Human Diseases > Infectious diseases: Bacterial > Bacterial invasion of epithelial cells.

· Human Diseases > Infectious diseases: Bacterial > Pathogenic Escherichia coli infection.

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

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

· Human Diseases > Cancers: Overview > Viral carcinogenesis.

· Human Diseases > Cancers: Overview > Proteoglycans in cancer.

· Human Diseases > Cancers: Overview > MicroRNAs in cancer.

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

· Organismal Systems > Immune system > Chemokine signaling pathway.   (View pathway)

· Organismal Systems > Circulatory system > Vascular smooth muscle contraction.   (View pathway)

· Organismal Systems > Development > Axon guidance.   (View pathway)

· Organismal Systems > Immune system > Platelet activation.   (View pathway)

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

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

· Organismal Systems > Immune system > Leukocyte transendothelial migration.   (View pathway)

· Organismal Systems > Nervous system > Neurotrophin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Oxytocin signaling pathway.

· Organismal Systems > Digestive system > Pancreatic secretion.

文献引用

1). Drop-shaped microgrooves guide unidirectional cell migration for enhanced endothelialization. Nature communications, 2025 (PubMed: 39994203) [IF=16.6]

2). MTH1 protects platelet mitochondria from oxidative damage and regulates platelet function and thrombosis. Nature Communications, 2023 (PubMed: 37563135) [IF=16.6]

Application: WB    Species: Mouse    Sample:

Fig. 4 Dysregulated protein phosphorylation in MTH1-deficient platelets after thrombin stimulation. a MTH1fl/fl or MTH1−/− platelets were treated with thrombin (1 U/ml) for 3 min followed by quantitative phosphoproteomics assay. b Differentially expressed phosphopeptides between two groups were presented as volcano map. X-axis shows the fold change (logarithmic conversion based on 2) and Y-axis shows the P-value (logarithmic conversion based on 10). Red dots represented the differentially upregulated phosphopeptides with significance and Blue dots showed the differentially downregulated phosphopeptides with significance. KEGG pathway analysis between control and MTH1-deficient platelets under the condition of resting (MA/NA) (c) or stimulation (MB/NB) (d). e MTH1fl/fl or MTH1−/− platelets were stimulated with thrombin (1 U/ml) followed by measuring the phosphorylation level of p38 MAPK, AKT, PLCβ3 and RhoA. The data were quantified based on three independent experiments (mean ± SD, n = 3 independent isolated platelets, two-way ANOVA with Sidak multiple comparisons test). f The number of differentially expressed phosphopeptides among the four groups. g Details of the 2 differentially expressed phosphopeptides localized in the mitochondria with significance identified from the comparison of control and MTH1-deficient platelets after thrombin stimulation (n = 3 independent experiments, two-tailed unpaired Student’s t test).

3). Targeting Phactr4 to rescue chronic stress-induced depression-like behavior in rats via regulating neuroinflammation and neuroplasticity. International journal of biological macromolecules, 2024 (PubMed: 38838879) [IF=7.7]

4). Mechanism of delayed encephalopathy after acute carbon monoxide poisoning. Neural Regeneration Research, 2020 (PubMed: 32594050) [IF=5.9]

5). Comparative Phosphoproteomics of Neuro-2a Cells under Insulin Resistance Reveals New Molecular Signatures of Alzheimer’s Disease. International Journal of Molecular Sciences, 2022 (PubMed: 35055191) [IF=5.6]

Application: WB    Species: Mice    Sample:

Figure 5 Comparative informatic analysis of phosphoproteomes of two different insulin-resistant conditions. (A) Comparative canonical pathway analysis between the phosphoproteomes. The positive and negative z-scores are shown in orange and blue, respectively. “Pal” and “TNF” indicate palmitate-induced insulin-resistant and TNF-α-induced insulin-resistant conditions, respectively. (B) The integrin pathway was the most downregulated pathway between the phosphoproteomes. The increased and decreased phosphorylation levels are shown in red and green, respectively. The red circles indicate the phosphoproteins commonly regulated by different insulin-resistant conditions. (C) Western blot of phospho-RhoA under palmitate-induced insulin-resistant conditions. Conditioned cell lysates were electrophoresed and blotted. “Insulin” indicates 100 nM of insulin treatment for 10 min. (D) The adenosine monophosphate-activated protein kinase pathway was the most downregulated pathway between the phosphoproteomes. (E) Western blot of phospho-protein kinase B and phospho-acetyl-CoA carboxylase under different insulin-resistant conditions. Conditioned cell lysates were electrophoresed and blotted. “Insulin” indicates 100 nM of insulin treatment for 10 min. (F) Comparative analysis for disease relation and biological functions. The positive and negative z-scores are shown in orange and blue color, respectively. “Pal” and “TNF” indicate palmitate-induced insulin-resistant condition and TNF-α-induced insulin-resistant condition, respectively.

6). Baicalin Attenuates Panton-Valentine Leukocidin (PVL)-Induced Cytoskeleton Rearrangement via Regulating the RhoA/ROCK/LIMK and PI3K/AKT/GSK-3β Pathways in Bovine Mammary Epithelial Cells. International journal of molecular sciences, 2023 (PubMed: 37833969) [IF=5.6]

Application: WB    Species: bovine    Sample: BMECs

Figure 3. Effects of rPVL on the regulation of RhoA/ROCK/LIMK/Cofilin and PI3K/AKT/GSK-3β signaling pathways and phosphorylation of cofilin and tau hyperphosphorylation in the rPVL-treated BMECs. Representative immunoblot bands for RhoA, p-ROCK2(Tyr722), ROCK2, p-LIMK1/2(Thr508/Thr505), p-cofilin (Ser3), and cofilin (A); p-PI3K (Tyr458/Tyr199), PI3K, p-AKT(Ser473), AKT, GSK-3β(Ser9), GSK-3β, p-tau (Ser396), and tau (B); GAPDH was used as a control. rPVL was used at a 100 ng/mL concentration. Data are expressed as mean ± standard deviation of three independent experiments. * 0.01 < p < 0.05, ** p < 0.01 (one-way ANOVA with Dunnett’s multiple comparison tests), ns: not significant.

7). Bisphenol A disrupts the neuronal F-actin cytoskeleton by activating the RhoA/ROCK/LIMK pathway in Neuro-2a cells. Toxicology, 2024 (PubMed: 39527977) [IF=4.8]

8). Heat treatment of galangin and kaempferol inhibits their benefits to improve barrier function in rat intestinal epithelial cells: Galangin & kaempferol improve IEC-6 cells barrier function. The Journal of Nutritional Biochemistry, 2021 (PubMed: 33011286) [IF=4.8]

9). Endostatin attenuates PDGF-BB- or TGF-β1-induced HSCs activation via suppressing RhoA/ROCK1 signal pathways. Drug Design Development and Therapy, 2019 (PubMed: 30666090) [IF=4.7]

Application: WB    Species: rat    Sample: HSC-T6 cells

Figure 4 |Endostatin inhibits the expression of α-SMA, RhoA, and ROCK1 at mRNA level.Notes: Transcript levels of α-SMA, RhoA, and ROCK1 were analyzed by RT-PCR (A–C). Endostatin significantly suppressed the expressions of α-SMA, RhoA, and ROCK1 at mRNA level in HSC-T6 cells. Data are expressed as mean ± SD. **P,0.01 (n=3 per group).

10). Galectin-3 exacerbates ox-LDL-mediated endothelial injury by inducing inflammation via integrin β1-RhoA-JNK signaling activation. JOURNAL OF CELLULAR PHYSIOLOGY, 2019 (PubMed: 30536538) [IF=4.5]

Application: WB    Species: human    Sample: HUVECs cells

FIGURE 4 | Gal‐3 increases the expression of integrin β1, GTP‐RhoA and p‐JNK in ox‐LDL induced HUVECs. After exposure to Gal‐3, ox‐LDL or their combination, the expression of integrin β1 was detected by IF, (a) WB was used to measure the protein levels of integrin β1, RhoA, JNK,GTP‐RhoA, and p‐JNK (b). The relative protein expression was further indicated using histograms (c). **p < 0.01, ##p < 0.01

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