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Learn37-2300
antibody from Invitrogen Antibodies
Targeting: CSPG4
CSPG4A, HMW-MAA, MCSP, MCSPG, MEL-CSPG, MSK16, NG2
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- Antigen structure
- References [4]
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- Product number
- 37-2300 - Provider product page
- Provider
- Invitrogen Antibodies
- Product name
- NG2 Monoclonal Antibody (N143.8)
- Antibody type
- Monoclonal
- Antigen
- Purifed from natural sources
- Reactivity
- Human, Rat
- Host
- Mouse
- Isotype
- IgG
- Antibody clone number
- N143.8
- Vial size
- 100 µg
- Concentration
- 0.5 mg/mL
- Storage
- -20°C
Submitted references IL-17 Inhibits Oligodendrocyte Progenitor Cell Proliferation and Differentiation by Increasing K(+) Channel Kv1.3.
Preclinical safety of human embryonic stem cell-derived oligodendrocyte progenitors supporting clinical trials in spinal cord injury.
Early proliferation does not prevent the loss of oligodendrocyte progenitor cells during the chronic phase of secondary degeneration in a CNS white matter tract.
Axon growth across a lesion site along a preformed guidance pathway in the brain.
Liu H, Yang X, Yang J, Yuan Y, Wang Y, Zhang R, Xiong H, Xu Y
Frontiers in cellular neuroscience 2021;15:679413
Frontiers in cellular neuroscience 2021;15:679413
Preclinical safety of human embryonic stem cell-derived oligodendrocyte progenitors supporting clinical trials in spinal cord injury.
Priest CA, Manley NC, Denham J, Wirth ED 3rd, Lebkowski JS
Regenerative medicine 2015 Nov;10(8):939-58
Regenerative medicine 2015 Nov;10(8):939-58
Early proliferation does not prevent the loss of oligodendrocyte progenitor cells during the chronic phase of secondary degeneration in a CNS white matter tract.
Payne SC, Bartlett CA, Savigni DL, Harvey AR, Dunlop SA, Fitzgerald M
PloS one 2013;8(6):e65710
PloS one 2013;8(6):e65710
Axon growth across a lesion site along a preformed guidance pathway in the brain.
Jin Y, Ziemba KS, Smith GM
Experimental neurology 2008 Apr;210(2):521-30
Experimental neurology 2008 Apr;210(2):521-30
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- Invitrogen Antibodies (provider)
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- Experimental details
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- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- FIGURE 5 Kv1.3 blockade protected corpus callosum from LPC-induced demyelination in vivo . The frozen sections were obtained from the demyelination model induced by stereotaxic injection of LPC (two points, 1%, 1 muL of each point) in corpus callosum. Mice were treated with or without PAP (6 mg/kg) and accepted BrdU (50 mg/kg) by i.p. injection. (A) Representative images of myelin sheath LFB staining (blue) in coronal sections of animal brain tissues. The low-magnification views (first line) show the complete coronal section, in which the framed parts are enlarged into the high-magnification views showing below. Compared with sham group, the injection site of LPC reduced significantly in overall density of staining for myelin. PAP significantly improved the LPC-induced myelin damage. (B) Western blot analysis of MBP expression in brain tissues around the injected points dissected out from the brain. The band marked by the arrow is a protein band with a size of 18.5 kDa. Blockade of Kv1.3 significantly prevented corpus callosum from LPC-induced MBP reduction ( n = 3). (C) Representative images of merged BrdU immunofluorescence staining (red), NG2 (green), and DAPI (blue) in sections. There were 10 randomly selected visual fields counted for each experimental group from three independent treatments. Cell density of BrdU + NG2 + cells are shown in the bar graph (right). The LPC-induced decrease in BrdU + NG2 + cells density was mitigated by PAP. * P < 0.05 vs. sham, *** P < 0.00
