SAB4200130
Anti-Phospholipase A2 (iPLA2) (C-terminal region) antibody produced in rabbit
~1.5 mg/mL, affinity isolated antibody
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Anti-CaI-PLA2, Anti-INAD1, Anti-IPLA2-VIA, Anti-PARK14, Anti-PLA2, Anti-PLA2G6, Anti-PNPLA9, Anti-Phospholipase A2, group VI (cytosolic, calcium-independent), GVI
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生物来源
rabbit
偶联物
unconjugated
抗体形式
affinity isolated antibody
抗体产品类型
primary antibodies
克隆
polyclonal
形式
buffered aqueous solution
分子量
antigen ~85 kDa
antigen ~95 kDa
种属反应性
mouse, human, rat
包装
antibody small pack of 25 μL
增强验证
recombinant expression
Learn more about Antibody Enhanced Validation
浓度
~1.5 mg/mL
技术
western blot: 1-2 μg/mL using extract of HEK-293T cells overexpressing human iPLA2, and 1-2 mg/mL using rat kidney extract (S1 fraction).
western blot: 1-2 μg/mL using rat kidney extract (S1 fraction)
UniProt登记号
运输
dry ice
储存温度
−20°C
靶向翻译后修饰
unmodified
基因信息
human ... PLA2G6(8398)
一般描述
Ca2+-independent phospholipase A2 (iPLA2), also known as PLA2G6, is a member of the PLA2 superfamily. It consists of a C-terminal calmodulin-binding domain, a bipartite nuclear localization sequence, GXSXG serine lipase residues, and ankyrin repeats at the N-terminus. iPLA2 gene is mapped to human chromosome 22q13.1 and encodes alternatively spliced isoforms.
特异性
Anti-Phospholipase A2 (iPLA2) (C-terminal region), specifically recognizes human and rat iPLA2.
应用
Anti-Phospholipase A2 (iPLA2) (C-terminal region) antibody produced in rabbit has been used in immunoblotting.
生化/生理作用
Ca2+-independent phospholipase A2 (iPLA2) catalyzes the cleavage of fatty acids from the sn-2 position of phospholipids. iPLA2 is implicated in leukotriene and prostaglandin production as well as in arachidonic acid release phospholipid remodeling. Mutations in the PLA2G6 gene are the cause of two childhood neurologic disorders, neurodegeneration with brain iron accumulation (NBIA) and infantile neuroaxonal dystrophy 1 (INAD1). Recent evidence suggests that both Ca2+-dependent PLA2 (cPLA2) and iPLA2 may play a central role in memory deficits at early stages.
外形
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
储存及稳定性
Store at −20 °C. For continuous use, the product may be stored at 2−8 °C for up to one month. For extended storage, freeze at −20 °C in working aliquots. Repeated freezing and thawing, or storage in “frost-free” freezers, is not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation. Discard working dilutions if not used within 12 hours.
免责声明
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
常规特殊物品
PloS one, 6(10), e26991-e26991 (2011-11-03)
Infantile neuroaxonal dystrophy (INAD) is a progressive, autosomal recessive neurodegenerative disease characterized by axonal dystrophy, abnormal iron deposition and cerebellar atrophy. This disease was recently mapped to PLA2G6, which encodes group VI Ca(2+)-independent phospholipase A(2) (iPLA(2) or iPLA(2)β). Here we
Psychopharmacology, 198(1), 1-27 (2008-04-09)
Alzheimer disease (AD), a progressive neurodegenerative disorder, is the leading cause of dementia in the elderly. A combination of cholinergic and glutamatergic dysfunction appears to underlie the symptomatology of AD, and thus, treatment strategies should address impairments in both systems.
PloS one, 5(9), e12897-e12897 (2010-10-05)
Mutations in the PLA2G6 gene have been identified in autosomal recessive neurodegenerative diseases classified as infantile neuroaxonal dystrophy (INAD), neurodegeneration with brain iron accumulation (NBIA), and dystonia-parkinsonism. These clinical syndromes display two significantly different disease phenotypes. NBIA and INAD are
Journal of medical genetics, 53(3), 180-189 (2015-12-17)
Mutations in PLA2G6, which encodes the calcium-independent phospholipase A2 group VI, cause neurodegeneration and diffuse cortical Lewy body formation by a yet undefined mechanism. We assessed whether altered protein glycosylation due to abnormal Golgi morphology might be a factor in
PLA2G6, encoding a phospholipase A2, is mutated in neurodegenerative disorders with high brain iron.
Nature genetics, 38(7), 752-754 (2006-06-20)
Neurodegenerative disorders with high brain iron include Parkinson disease, Alzheimer disease and several childhood genetic disorders categorized as neuroaxonal dystrophies. We mapped a locus for infantile neuroaxonal dystrophy (INAD) and neurodegeneration with brain iron accumulation (NBIA) to chromosome 22q12-q13 and
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