MAB5502
Anti-Vesicular Glutamate Transporter 1 Antibody
CHEMICON®, mouse monoclonal, 3C10.2
Szinonimák:
Solute carrier family 17 member 7, Brain-specific Na(+)-dependent inorganic phosphate cotransporter, vGluT1
Bejelentkezésa Szervezeti és Szerződéses árazás megtekintéséhez
Összes fotó(3)
About This Item
UNSPSC kód:
12352203
eCl@ss:
32160702
NACRES:
NA.41
klón:
3C10.2, monoclonal
application:
IHC
WB
WB
faj reaktivitás:
mouse
technika/technikák:
immunohistochemistry: suitable
western blot: suitable
western blot: suitable
citations:
76
Javasolt termékek
Terméknév
Anti-Vesicular Glutamate Transporter 1 Antibody, clone 3C10.2, Chemicon®, from mouse
biológiai forrás
mouse
Minőségi szint
antitest forma
purified immunoglobulin
antitest terméktípus
primary antibodies
klón
3C10.2, monoclonal
faj reaktivitás
mouse
faj reaktivitás (homológia által előrejelzett)
rat
gyártó/kereskedő neve
Chemicon®
technika/technikák
immunohistochemistry: suitable
western blot: suitable
izotípus
IgG1
NCBI elérési szám
UniProt elérési szám
kiszállítva
wet ice
célzott transzláció utáni módosítás
unmodified
Géninformáció
rat ... Slc17A7(116638)
Általános leírás
VGLUT1 is expressed in a subset of glutamate neurons and transports glutamate into native synaptic vesicles from the brain, exhibiting a conductance for chloride that is blocked by glutamate. Vesicular glutamate transport has a substantially lower apparent affinity than the plasma membrane excitatory amino acid transporters. Glutamate transport by VGLUT1 is saturated with a K(m) of approximately 2 mM, in the same range as transport by synaptic vesicles. Finally, plasma membrane glutamate transporters recognize both aspartate and glutamate as substrates, whereas VGLUT1 does not recognize aspartate. Vesicular glutamate transporters pack the neurotransmitter into synaptic vesicles so that they can be released into the synapse. VGLUTs are dependent on a proton gradient that they create by hydrolysing adenosine triphosphate (ATP). VGLUTs have only between one hundredth and one thousandth the affinity for glutamate that EAATs have.
Egyediség
Reacts with VGLUT1 (Vesicular Glutamate Transporter 1).
Immunogén
Recombinant protein from rat VGLUT1.
Alkalmazás
Immunohistochemistry:
A previous lot of this antibody was tested on IH.
Optimal working dilutions must be determined by end user.
A previous lot of this antibody was tested on IH.
Optimal working dilutions must be determined by end user.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Ion Channels & Transporters
Neuronal & Glial Markers
Ion Channels & Transporters
Neuronal & Glial Markers
This Anti-Vesicular Glutamate Transporter 1 Antibody, clone 3C10.2, Cat. No. MAB5502, is validated for use in IH, WB for the detection of VGluT1.
Minőség
Routinely evaluated by Western Blot on Mouse Brain lysates.
Western Blot Analysis:
1:500 dilution of this lot detected Vesicular Glutamate Transporter 1 on 10 μg of Mouse Brain lysates.
Western Blot Analysis:
1:500 dilution of this lot detected Vesicular Glutamate Transporter 1 on 10 μg of Mouse Brain lysates.
Cél megnevezése
60 kDa
Fizikai forma
Format: Purified
Protein A purified
Purified mouse monoclonal IgG1 in buffer containing PBS containing 0.1% sodium azide.
Tárolás és stabilitás
Stable for 6 months at 2-8ºC in undiluted aliquots from date of receipt.
Analízis megjegyzés
Control
Brain
VGLUT1 Control Peptide AG208
Brain
VGLUT1 Control Peptide AG208
Egyéb megjegyzések
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Jogi információk
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
Jogi nyilatkozat
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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Tárolási osztály kódja
12 - Non Combustible Liquids
WGK
WGK 2
Lobbanási pont (F)
Not applicable
Lobbanási pont (C)
Not applicable
Analitikai tanúsítványok (COA)
Analitikai tanúsítványok (COA) keresése a termék sarzs-/tételszámának megadásával. A sarzs- és tételszámok a termék címkéjén találhatók, a „Lot” vagy „Batch” szavak után.
Már rendelkezik ezzel a termékkel?
Az Ön által nemrégiben megvásárolt termékekre vonatkozó dokumentumokat a Dokumentumtárban találja.
April P Neal et al.
Toxicological sciences : an official journal of the Society of Toxicology, 116(1), 249-263 (2010-04-09)
Lead (Pb(2+)) exposure is known to affect presynaptic neurotransmitter release in both in vivo and cell culture models. However, the precise mechanism by which Pb(2+) impairs neurotransmitter release remains unknown. In the current study, we show that Pb(2+) exposure during
Mizuya Shinoyama et al.
Frontiers in cellular neuroscience, 7, 128-128 (2013-08-24)
Hypoxic-ischemic encephalopathy (HIE) at birth could cause cerebral palsy (CP), mental retardation, and epilepsy, which last throughout the individual's lifetime. However, few restorative treatments for ischemic tissue are currently available. Cell replacement therapy offers the potential to rescue brain damage
Kajari Karmakar et al.
Cell reports, 18(1), 185-197 (2017-01-05)
Tonotopy is a hallmark of auditory pathways and provides the basis for sound discrimination. Little is known about the involvement of transcription factors in brainstem cochlear neurons orchestrating the tonotopic precision of pre-synaptic input. We found that in the absence
M M Hamza et al.
Molecular neurobiology, 53(8), 5203-5216 (2015-09-25)
The cerebellum is a structure of the central nervous system involved in balance, motor coordination, and voluntary movements. The elementary circuit implicated in the control of locomotion involves Purkinje cells, which receive excitatory inputs from parallel and climbing fibers, and
Pietro Fazzari et al.
eLife, 3 (2014-06-04)
Neuregulin 1 (NRG1) and the γ-secretase subunit APH1B have been previously implicated as genetic risk factors for schizophrenia and schizophrenia relevant deficits have been observed in rodent models with loss of function mutations in either gene. Here we show that
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