MABN1190
Anti-DLG4 Antibody
mouse monoclonal, 1A8.1
Szinonimák:
Disks large homolog 4, Postsynaptic density protein 95, PSD-95, Synapse-associated protein 90, SAP-90, SAP90
Bejelentkezésa Szervezeti és Szerződéses árazás megtekintéséhez
Összes fotó(2)
About This Item
UNSPSC kód:
12352203
eCl@ss:
32160702
NACRES:
NA.41
klón:
1A8.1, monoclonal
application:
IHC
WB
WB
faj reaktivitás:
rat, human
technika/technikák:
immunohistochemistry: suitable
western blot: suitable
western blot: suitable
citations:
5
Javasolt termékek
Terméknév
Anti-PSD95 Antibody, clone 1A8.1, clone 1A8.1, from mouse
biológiai forrás
mouse
Minőségi szint
antitest forma
purified immunoglobulin
antitest terméktípus
primary antibodies
klón
1A8.1, monoclonal
faj reaktivitás
rat, human
technika/technikák
immunohistochemistry: suitable
western blot: suitable
izotípus
IgG1κ
NCBI elérési szám
UniProt elérési szám
célzott transzláció utáni módosítás
unmodified
Géninformáció
human ... DLG4(1742)
Általános leírás
Disks large homolog 4 (UniProt P78352; also known as Postsynaptic density protein 95, PSD-95, SAP-90, SAP90, Synapse-associated protein 90) is encoded by the DLG4 (also known as PSD95) gene (Gene ID 1742) in human. PSD-95 belong to the family of membrane-associated guanylate kinases (MAGUKs), which also include PSD-93, SAP97 and SAP102. PSD95 is predominantly expressed in the hippocampus CA1 region and prefrontal cortex of the brain, where it localizes in a somatodendritic pattern in the post-synaptic membrane and in presynaptic axon terminals of inhibitory neurons. PDS-95 is the major scaffolding protein in the excitatory postsynaptic density (PSD) and a potent regulator of synaptic strength via interactions with a diverse PSD proteins, including NMDA receptors (NMDARs), AMPA receptor (AMPAR) complexes via Stargazin/TARP, adhesion molecules, as well as other scaffolding proteins, such as GKAP and Shank. PSD95 and neuronal nitric-oxide synthase (nNOS) interaction plays a role in maintaining hypersensitivity in acute and chronic pain. In addition, the assembly of the GluR6-PSD95-CaMKII complex is implicated as a majore signaling module that mediates injury induced by brain ischemia by facilitating GluR6 serine phosphorylation by CaMKII and the activation of JNK.
Egyediség
Clone 1A8.1 epitope sequence is present in all spliced isoforms of human, mouse, and rat PSD95 reported by UniProt (P78352, Q62108, P31016).
Immunogén
Epitope: Region between PDZ domain 2 & 3.
KLH-conjugated linear peptide corresponding to the region between PDZ domain 2 & 3 of human PSD95.
Alkalmazás
Anti-PSD95 Antibody, clone 1A8.1 is an antibody against PSD95 for use in Western Blotting, Immunohistochemistry.
Immunohistochemistry Analysis: A 1:50 dilution from a representative lot PSD95 in human cerebral cortex and cerebellum tissue sections.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Synapse & Synaptic Biology
Synapse & Synaptic Biology
Minőség
Evaluated by Western Blotting in rat hippocampus tissue lysate.
Western Blotting Analysis: 0.5 µg/mL of this antibody detected PSD95 in 10 µg of rat hippocampus tissue lysate.
Western Blotting Analysis: 0.5 µg/mL of this antibody detected PSD95 in 10 µg of rat hippocampus tissue lysate.
Cél megnevezése
~80 kDa observed. 80.50/80.47/80.47 kDa human/mouse/rat isoform 1; PSD95-alpha), 85.43/85.42 kDa (human/mouse isoform 2; PSD95-beta), 80.13/80.10 kDa (human/mouse isoform 3) calculated.
Fizikai forma
Format: Purified
Protein G purified.
Purified mouse monoclonal IgG1κ antibody in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
Tárolás és stabilitás
Stable for 1 year at 2-8°C from date of receipt.
Egyéb megjegyzések
Concentration: Please refer to lot specific datasheet.
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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javasolt
Tárolási osztály kódja
12 - Non Combustible Liquids
WGK
WGK 1
Lobbanási pont (F)
Not applicable
Lobbanási pont (C)
Not applicable
Analitikai tanúsítványok (COA)
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Beatrice Vignoli et al.
Cells, 11(9) (2022-05-15)
Neurons release and respond to brain-derived neurotrophic factor (BDNF) with bursts of brain activity. BDNF action is known to extend to peri-synaptic astrocytes, contributing to synaptic strengthening. This implies that astrocytes have a set of dynamic responses, some of which
Angela O Dorigatti et al.
GeroScience, 43(1), 115-124 (2020-10-17)
The ability to generate in vitro cultures of neuronal cells has been instrumental in advancing our understanding of the nervous system. Rodent models have been the principal source of brain cells used in primary cultures for over a century, providing
Yuying Huang 黄玉莹 et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 44(4) (2023-12-21)
K+-Cl- cotransporter-2 (KCC2) critically controls neuronal chloride homeostasis and maintains normal synaptic inhibition by GABA and glycine. Nerve injury diminishes synaptic inhibition in the spinal cord via KCC2 impairment. However, how KCC2 regulates nociceptive input to spinal excitatory and inhibitory
Daozhong Jin et al.
Journal of neurochemistry, 164(2), 143-157 (2022-10-13)
Glutamate NMDA receptors (NMDARs) in the nucleus accumbens (NAc) are critically involved in drug dependence and reward. α2δ-1 is a newly discovered NMDAR-interacting protein that promotes synaptic trafficking of NMDARs independently of its conventional role as a calcium channel subunit.
Daozhong Jin et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 43(31), 5593-5607 (2023-07-15)
Aberrant activation of presynaptic NMDARs in the spinal dorsal horn is integral to opioid-induced hyperalgesia and analgesic tolerance. However, the signaling mechanisms responsible for opioid-induced NMDAR hyperactivity remain poorly identified. Here, we show that repeated treatment with morphine or fentanyl
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