PCK1 Antibody - #DF6770

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产品: PCK1 抗体
货号: DF6770
描述: Rabbit polyclonal antibody to PCK1
应用: WB IHC IF/ICC
文献验证: WB, IF/ICC
反应: Human, Mouse, Rat
预测: Bovine, Sheep, Rabbit, Dog
蛋白号: P35558
RRID: AB_2838732

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 50ul RMB¥ 1250 现货
 100ul RMB¥ 2300 现货
 200ul RMB¥ 3000 现货

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实验方案
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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
克隆:
Polyclonal
特异性:
PCK1 Antibody detects endogenous levels of total PCK1.
RRID:
AB_2838732
引用格式: Affinity Biosciences Cat# DF6770, RRID:AB_2838732.
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

cytosolic [GTP]; GTP; PCK1; PCKGC_HUMAN; PEP carboxykinase; PEPCK-C; PEPCK1; PEPCKC; Phosphoenolpyruvate carboxykinase 1 (soluble); Phosphoenolpyruvate carboxykinase 1; Phosphoenolpyruvate carboxykinase; Phosphoenolpyruvate carboxykinase, cytosolic [GTP]; Phosphoenolpyruvate carboxykinase, cytosolic; Phosphoenolpyruvate carboxylase; Phosphopyruvate carboxylase;

抗原和靶标

免疫原:

A synthesized peptide derived from human PCK1, corresponding to a region within C-terminal amino acids.

基因/基因ID:
PCK1(5105)
描述:
PCK1(Phosphoenolpyruvate carboxykinase, cytosolic) is also named as PEPCK1 and belongs to the phosphoenolpyruvate carboxykinase [GTP] family. It catalyzes the formation of phosphoenolpyruvate from oxaloacetate, with the release of carbon dioxide and GDP. It is also a main control point for the regulation of gluconeogenesis. In eukaryotes there are two isozymes: a cytoplasmic one and a mitochondrial one. Defects in PCK1 are the cause of cytosolic phosphoenolpyruvate carboxykinase deficiency (C-PEPCKD). This antibody is specific to PCK1.

研究领域

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

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

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

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Metabolism > Carbohydrate metabolism > Glycolysis / Gluconeogenesis.

· Metabolism > Carbohydrate metabolism > Citrate cycle (TCA cycle).

· Metabolism > Carbohydrate metabolism > Pyruvate metabolism.

· Metabolism > Global and overview maps > Metabolic pathways.

· Organismal Systems > Endocrine system > PPAR signaling pathway.

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

· Organismal Systems > Endocrine system > Adipocytokine signaling pathway.

· Organismal Systems > Endocrine system > Glucagon signaling pathway.

· Organismal Systems > Excretory system > Proximal tubule bicarbonate reclamation.

文献引用

1). Retinal metabolism displays evidence for uncoupling of glycolysis and oxidative phosphorylation via Cori-, Cahill-, and mini-Krebs-cycle. eLife, 2024 (PubMed: 38739438) [IF=6.4]

Application: IF/ICC    Species: Mouse    Sample:

Figure 6. Metabolomic comparison between control, 1,9-dideoxyforskolin (1,9-DDF), and carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP) treatment. (A) Heatmap illustrating 29 statistically significant metabolite changes (parametric one-way ANOVA, Fisher’s LSD post hoc analysis). Three main clusters of metabolite changes were evident (dashed lines). (B) Immunostaining (green) for enzymes related to glutamine metabolism. DAPI (grey) was used as nuclear counterstain. (B1) Glutamine synthase (GS), (B2) glutaminase C (GAC); co-localisation with cone-arrestin (Arr3; magenta). (B3) Phosphoenolpyruvate carboxykinase 1 (PCK1) did not co-localise with cone marker peanut agglutinin (PNA) while (B4) PCK2 did. (C) Ratios between metabolites representing glycolysis (lactate vs. guanosine triphosphate [GTP]), anaplerotic metabolism (GTP vs. branched chain amino acids [BCAA]), and serine synthesis pathway (serine vs. lactate). Data represented as individual data points with mean ± SD (n=5).
2). Nr2e1 ablation impairs liver glucolipid metabolism and induces inflammation, high-fat diets amplify the damage. Biomedicine & Pharmacotherapy, 2019 (PubMed: 31590127) [IF=4.0]

Application: WB    Species: mouse    Sample: liver

Fig. 3. |Nr2e1 deficiency impaired glucose tolerance and insulin sensitivity, the damages were exacerbated by HFD.Western blots measured the expression of phosphorylated protein of IRS1, AKT, GSK3β and FOXO1 in the liver samples after 12 weeks of HFD or SD feeding (3 H). Phosphorylated protein levels were normalized to the respective total protein levels (3I).
3). Mechanism of N-Methyl-N-Nitroso-Urea-Induced Gastric Precancerous Lesions in Mice. Journal of Oncology, 2022 (PubMed: 35342404)
4). Mechanism of Hypoxia-Activated MiR-194 /FoxO3a Inducing Glycolytic Metabolism Reprogramming in Gastric Precancerous Lesions. Research Square, 2021

Application: WB    Species: Mouse    Sample: gastric mucosa

Figure 6. Changes in expression levels of key proteins in the FoxO3a signaling pathway in Figure 6. Changes in expression levels of key proteins in the FoxO3a signaling pathway in gastric mucosa. A, immunoblot showing protein expression levels of P-FoxO3a, FoxO3a, P-AMPK, AMPK, PCK1, LKB1, and LDHA. B, The ratio of P-FoxO3a/FoxO3a is lower, P-AMPK/AMPK and P-AKT/AKT are higher in GPL.C, The PCK1, LKB1 decreased, and LDHA overexpressed in GPL,. A, immunoblot showing protein expression levels of P-FoxO3a, FoxO3a, P-AMPK, AMPK, PCK1, LKB1, and LDHA. B, The ratio of P-FoxO3a/FoxO3a is lower, P-AMPK/AMPK and P-AKT/AKT are higher in GPL.C, The PCK1, LKB1 decreased, and LDHA overexpressed in GPL,
5). The retina uncouples glycolysis and oxidative phosphorylation via Cori-, Cahill-, and mini-Krebs-cycle. bioRxiv, 2023

Application: IF/ICC    Species: Fish    Sample:

Figure 10 Metabolomic comparison between control, 1,9-DDF, and FCCP treatment. (A) Heatmap illustrating 29 statistically significant metabolite changes (parametric one-way ANOVA, Fisher’s LSD post-hoc analysis). Three main clusters of metabolite changes were evident (dashed lines). (B) Immunostaining (green) for enzymes related to glutamine metabolism. DAPI (grey) was used as nuclear counterstain. (B1) Glutamine synthase (GS), (B2) glutaminase C (GAC); co-localization with cone-arrestin (Arr3; magenta). (B3) phosphoenolpyruvate carboxykinase 1 (PCK1) did not co-localize with cone marker peanut-agglutinin (PNA) while (B4) PCK2 did. (C) Ratios between metabolites representing glycolysis (lactate vs. GTP), anaplerotic metabolism (GTP vs. BCAA), and serine synthesis pathway (serine vs. lactate). Data represented as individual data points with mean ± SD. Statistical testing: One-way ANOVA with Tukey’s post-hoc test; p-values: **** < 0.0001, *** < 0.001, ** < 0.01 * < 0.05. See also Supplementary.

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