SAB4200130
Anti-Phospholipase A2 (iPLA2) (C-terminal region) antibody produced in rabbit
~1.5 mg/mL, affinity isolated antibody
别名:
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
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen ~85 kDa, antigen ~95 kDa
species reactivity
mouse, human, rat
packaging
antibody small pack of 25 μL
enhanced validation
recombinant expression
Learn more about Antibody Enhanced Validation
concentration
~1.5 mg/mL
technique(s)
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 accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... PLA2G6(8398)
General description
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.
Application
Anti-Phospholipase A2 (iPLA2) (C-terminal region) antibody produced in rabbit has been used in immunoblotting.
Biochem/physiol Actions
Anti-Phospholipase A2 (iPLA2) (C-terminal region), specifically recognizes human and rat iPLA2.
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.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Preparation Note
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.
Disclaimer
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.
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存储类别
10 - Combustible liquids
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
常规特殊物品
常规特殊物品
低风险生物材料
此项目有
Zhengshan Zhao et al.
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
Laura A Engel et al.
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
Evelin L Schaeffer et al.
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.
Govind Gupta et al.
ACS nano, 17(17), 17451-17467 (2023-08-29)
Nanoparticles (NPs) elicit sterile inflammation, but the underlying signaling pathways are poorly understood. Here, we report that human monocytes are particularly vulnerable to amorphous silica NPs, as evidenced by single-cell-based analysis of peripheral blood mononuclear cells using cytometry by time-of-flight
Mariska Davids et al.
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
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