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| 產(chǎn)地 | 進口、國產(chǎn) |
| 品牌 | 上海莼試 |
| 保存條件 | Store at -20 °C |
| 貨號 | CS10188 |
| 應用范圍 | WB=1:100-500 ELISA=1:500-1000 IP=1:20-100 IHC-P=1:100-500 IHC-F=1:100-500 Flow-Cyt=1:100-500 IF=1:100-500 |
| CAS編號 | |
| 抗體名 | Anti-PDHA1/PDH-E1α |
| 克隆性 | |
| 靶點 | 詳見說明書 |
| 適應物種 | 詳見說明書 |
| 形態(tài) | 詳見說明書 |
| 宿主 | 詳見說明書 |
| 亞型 | IgG |
| 標識物 | 詳見說明書 |
| 濃度 | 1mg/1ml% |
| 免疫原 | KLH conjugated synthetic peptide derived from human PDHA1 |
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丙酮酸脫氫酶α1抗體說明書 英文名稱 Anti-PDHA1/PDH-E1α
中文名稱 丙酮酸脫氫酶α1抗體說明書
別 名 mitochondrial; somatic form; ODPA_HUMAN; PDH; PDHA1; PDHCE1A; PDHE1 A type I; PDHE1-A type I; PHE1A; Pyruvate Dehydrogenase (lipoamide) alpha 1; Pyruvate Dehydrogenase E1 alpha; Pyruvate dehydrogenase E1 component subunit alpha; Pyruvate dehydrogenase E1 component subunit alpha, somatic form, mitochondrial.
產(chǎn)品屬性：
濃 度 1mg/1ml
規(guī) 格 0.2ml/200μg
抗體來源 Rabbit
克隆類型 polyclonal
交叉反應 Human, Mouse, Rat, Chicken, Dog, Pig, Cow, Horse, Rabbit
產(chǎn)品類型 一抗
研究領域 細胞生物 免疫學 激酶和磷酸酶 線粒體
蛋白分子量 predicted molecular weight: 43kDa
性 狀 Lyophilized or Liquid
免 疫 原 KLH conjugated synthetic peptide derived from human PDHA1
亞 型 IgG
純化方法 affinity purified by Protein A
儲 存 液 0.01M PBS, pH 7.4 with 10 mg/ml BSA and 0.1% Sodium azide
丙酮酸脫氫酶α1抗體說明書 產(chǎn)品應用 WB=1:100-500 ELISA=1:500-1000 IP=1:20-100 IHC-P=1:100-500 IHC-F=1:100-500 Flow-Cyt=1:100-500 IF=1:100-500
（石蠟切片需做抗原修復）
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
保存條件 Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
Important Note This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
產(chǎn)品介紹 The pyruvate dehydrogenase (PDH) complex is a nuclear-encoded mitochondrial multienzyme complex that catalyzes the overall conversion of pyruvate to acetyl-CoA and CO(2), and provides the primary link between glycolysis and the tricarboxylic acid (TCA) cycle. The PDH complex is composed of multiple copies of three enzymatic components: pyruvate dehydrogenase (E1), dihydrolipoamide acetyltransferase (E2) and lipoamide dehydrogenase(E3). The E1 enzyme is a heterotetramer of two alpha and two beta subunits. This gene encodes the E1 alpha 1 subunit containing the E1 active site, and plays a key role in the function of the PDH complex. Mutations in this gene are associated with pyruvate dehydrogenase E1-alpha deficiency and X-linked Leigh syndrome. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
Function : The pyruvate dehydrogenase complex catalyzes the overall conversion of pyruvate to acetyl-CoA and CO(2), and thereby links the glycolytic pathway to the tricarboxylic cycle.
Subunit : Tetramer of 2 alpha and 2 beta subunits.
Subcellular Location : Mitochondrion matrix.
Post-translational modifications : Phosphorylation at Ser-232, Ser-293 and Ser-300 by PDK family kinases inactivates the enzyme; for this phosphorylation at a single site is sufficient. Dephosphorylation at all three sites, i.e. at Ser-232, Ser-293 and Ser-300, is required for reactivation.
DISEASE : Pyruvate dehydrogenase E1-alpha deficiency (PDHAD) [MIM:312170]: An enzymatic defect causing primary lactic acidosis in children. It is associated with a broad clinical spectrum ranging from fatal lactic acidosis in the newborn to chronic neurologic dysfunction with structural abnormalities in the central nervous system without systemic acidosis. Note=The disease is caused by mutations affecting the gene represented in this entry.
X-linked Leigh syndrome (X-LS) [MIM:308930]: Early-onset progressive neurodegenerative disorder with a characteristic neuropathology consisting of focal, bilateral lesions in one or more areas of the central nervous system, including the brainstem, thalamus, basal ganglia, cerebellum, and spinal cord. The lesions are areas of demyelination, gliosis, necrosis, spongiosis, or capillary proliferation. Clinical symptoms depend on which areas of the central nervous system are involved. The most common underlying cause is a defect in oxidative phosphorylation. LS may be a feature of a deficiency of any of the mitochondrial respiratory chain complexes. Note=The disease is caused by mutations affecting the gene represented in this entry.
Database links : UniProtKB/Swiss-Prot: P08559.3
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