产品编号 | bs-12079R-Gold |
英文名称1 | Rabbit Anti-phospho-GABRG2 (Ser366)/Gold Conjugated antibody |
中文名称 | 胶体金标记的磷酸化γ氨基丁酸γ2受体抗体 |
别 名 | p-GABAA Rγ2 (Ser 365); CAE 2; CAE2; ECA 2; ECA2; GABA(A) receptor subunit gamma 2; GABA(A) receptor subunit gamma-2; GABRG 2; GABRG2 antibody Gamma aminobutyric acid (GABA) A receptor gamma 2; Gamma aminobutyric acid A receptor gamma 2; Gamma aminobutyric acid receptor gamma 2 subunit; Gamma-aminobutyric acid receptor subunit gamma-2; Gamma-aminobutyric-acid receptor gamma-2 subunit; GBRG2_HUMAN; GEFSP 3; GEFSP3. |
规格价格 | 100ul/2980元 购买 大包装/询价 |
说 明 书 | 100ul(10nm 15nm 35nm) |
产品类型 | 磷酸化抗体 |
研究领域 | 神经生物学 通道蛋白 细胞膜受体 G蛋白偶联受体 G蛋白信号 |
抗体来源 | Rabbit |
克隆类型 | Polyclonal |
交叉反应 | Mouse, Rat, (predicted: Human, Chicken, Dog, Pig, Cow, Horse, Sheep, ) |
产品应用 | IEM=1:20-200 ICA=1:20-200 ChIP=1:20-200
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
分 子 量 | 50kDa |
性 状 | Lyophilized or Liquid |
浓 度 | 0.4mg/ml |
免 疫 原 | KLH conjugated synthesised phosphopeptide derived from human GABRG2 around the phosphorylation site of Ser366 |
亚 型 | IgG |
纯化方法 | affinity purified by Protein A |
储 存 液 | 0.02M TBS(pH8.2) with 1% BSA, 0.03% Proclin300. |
保存条件 | Store at 2-8 ºC for 3-6 months. Avoid repeated freeze/thaw cycles. |
产品介绍 |
background: GAD-65 and GAD-67, glutamate decarboxylases, function to catalyze the production of GABA (gamma-aminobutyric acid). In the central nervous system, GABA functions as the main inhibitory transmitter by increasing a Cl- (chloride) conductance that inhibits neuronal firing. GABA has been shown to activate both ionotropic (GABAA) and metabotropic (GABAB) receptors, as well as a third class of receptors called GABAC. The ?subunit of GABAA receptors are important for benzodiazepine binding and modulation of GABA-mediated Cl- current. GABAA R? is a 467 amino acid mulit-pass membrane protein localized to the postsynaptic cell membrane. Present as a pentamer with other GABAA receptor chains (Alpha, Beta, Gamma, Delta and Epsilon), the GABAA ligand-gated Cl- channels selectively complex with D5DR to enable mutual inhibitory functional interactions between the two receptor systems. Defects in the gene encoding GABAA R Gamma 2 have been found to be the cause of childhood absence epilepsy type 2, familial febrile convulsions type 8, generalized epilepsy with febrile seizures plus type 3 and severe myoclonic epilepsy in infancy. Function: GABA, the major inhibitory neurotransmitter in the vertebrate brain, mediates neuronal inhibition by binding to the GABA/benzodiazepine receptor and opening an integral chloride channel. Subunit: Generally pentameric. There are five types of GABA(A) receptor chains: alpha, beta, gamma, delta, and rho. Interacts with GABARAP. Subcellular Location: Cell junction, synapse, postsynaptic cell membrane; Multi-pass membrane protein. Cell membrane; Multi-pass membrane protein. Post-translational modifications: Palmitoylated by ZDHHC3/GODZ; which may affect presynaptic clustering and/or cell surface stability. DISEASE: Defects in GABRG2 are the cause of childhood absence epilepsy type 2 (ECA2) [MIM:607681]. ECA2 is a subtype of idiopathic generalized epilepsy (IGE) characterized by an onset at age 6-7 years, frequent absence seizures (several per day) and bilateral, synchronous, symmetric 3-Hz spike waves on EEG. During adolescence, tonic-clonic and myoclonic seizures develop. Some individuals manifest ECA2 occurring in combination with febrile convulsions. Defects in GABRG2 are the cause of familial febrile convulsions type 8 (FEB8) [MIM:611277]. A febrile convulsion is defined as a seizure event in infancy or childhood, usually occurring between 6 months and 6 years of age, associated with fever but without any evidence of intracranial infection or defined pathologic or traumatic cause. Febrile convulsions affect 5-12% of infants and children up to 6 years of age. There is epidemiological evidence that febrile seizures are associated with subsequent afebrile and unprovoked seizures in 2% to 7% of patients. Defects in GABRG2 are the cause of generalized epilepsy with febrile seizures plus type 3 (GEFS+3) [MIM:604233]. Generalized epilepsy with febrile seizures-plus refers to a rare autosomal dominant, familial condition with incomplete penetrance and large intrafamilial variability. Patients display febrile seizures persisting sometimes beyond the age of 6 years and/or a variety of afebrile seizure types. GEFS+ is a disease combining febrile seizures, generalized seizures often precipitated by fever at age 6 years or more, and partial seizures, with a variable degree of severity. Defects in GABRG2 are a cause of severe myoclonic epilepsy in infancy (SMEI) [MIM:607208]; also called Dravet syndrome. SMEI is a rare disorder characterized by generalized tonic, clonic, and tonic-clonic seizures that are initially induced by fever and begin during the first year of life. Later, patients also manifest other seizure types, including absence, myoclonic, and simple and complex partial seizures. Psychomotor development delay is observed around the second year of life. SMEI is considered to be the most severe phenotype within the spectrum of generalized epilepsies with febrile seizures-plus. Similarity: Belongs to the ligand-gated ion channel (TC 1.A.9) family. Gamma-aminobutyric acid receptor (TC 1.A.9.5) subfamily. GABRG2 sub-subfamily. Database links: Entrez Gene: 2566 Human Entrez Gene: 14406 Mouse Omim: 137164 Human SwissProt: P18507 Human SwissProt: P22723 Mouse Unigene: 7195 Human Unigene: 5309 Mouse Unigene: 159942 Rat Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
1、抗体溶解方法 | |
2、抗体修复方式 | |
3、常用试剂的配制 | |
4、免疫组化操作步骤 | |
5、免疫组化问题解答 | |
6、Western Blotting 操作步骤 | |
7、Western Blotting 问题解答 | |
8、关于肽链的设计 | |
9、多肽的溶解与保存 | |
10、酶标抗体效价测定程序 | |