Key Specifications Table
|Species Reactivity||Key Applications||Host||Format||Antibody Type|
|H, M, R||IHC||M||Purified||Monoclonal Antibody|
|Description||Anti-Nerve Growth Factor Receptor Antibody, clone MLR2|
|Presentation||Purified immunoglobulin. Lyophilized. Contains no preservative. Reconstitute with 100 μL of sterile distilled water.|
|Safety Information according to GHS|
|Material Size||100 µg|
|Reference overview||Pub Med ID|
|Chronic exposure to nerve growth factor increases acetylcholine and glutamate release from cholinergic neurons of the rat medial septum and diagonal band of Broca via mechanisms mediated by p75NTR. |
Huh, Carey Y L, et al.
J. Neurosci., 28: 1404-9 (2008) 2008
|Characterization and use of the NSC-34 cell line for study of neurotrophin receptor trafficking. |
Matusica, Dusan, et al.
J. Neurosci. Res., 86: 553-65 (2008) 2008
|Primary sensory neuron addition in the adult rat trigeminal ganglion: evidence for neural crest glio-neuronal precursor maturation. |
Lagares, Alfonso, et al.
J. Neurosci., 27: 7939-53 (2007) 2007
It is debated whether primary sensory neurons of the dorsal root ganglia increase the number in adult animals and, if so, whether the increase is attributable to postnatal neurogenesis or maturation of dormant, postmitotic precursors. Similar studies are lacking in the trigeminal ganglion (TG). Here we demonstrate by stereological methods that the number of neurons in the TG of adult male rats nearly doubles between the third and eighth months of age. The increase is mainly attributable to the addition of small, B-type neurons, with a smaller contribution of large, A-neurons. We looked for possible proliferative or maturation mechanisms that could explain this dramatic postnatal expansion in neuron number, using bromodeoxyuridine (BrdU) labeling, immunocytochemistry for neural precursor cell antigens, retrograde tracing identification of peripherally projecting neurons, and in vitro isolation of precursor cells from adult TG explant cultures. Cell proliferation identified months after an extended BrdU administration was sparse and essentially corresponded to glial cells. No BrdU-labeled cell took up the peripherally injected tracer, and only a negligible number coexpressed BrdU and the pan-neuronal tracer neuron-specific enolase. In contrast, a population of cells not recognizable as mature neurons in the TG and neighboring nerve expressed neuronal precursor antigens, and neural crest glioneuronal precursor cells were successfully isolated from adult TG explants. Our data suggest that a protracted maturation process persists in the TG that can be responsible for the neuronal addition found in the adult rat.
|Functional monoclonal antibodies to p75 neurotrophin receptor raised in knockout mice. |
Rogers, Mary-Louise, et al.
J. Neurosci. Methods, 158: 109-20 (2006) 2006
In this study, p75NTREXONIII knockout mice were used as immune-naive hosts to produce functional antibodies to human p75NTR. Three monoclonal antibodies were produced and named MLR1, MLR2 and MLR3, and isotyped as IgG1, IgG2a and IgG2a, respectively. MLR1 and MLR2 bound to human p75NTR with higher affinity than the well-characterized ME20.4 in ELISA and also recognized p75NTR present on neurons in both rat and mouse. MLR1 and MLR2 bound to nerves known to express p75NTR following injection into Balb/C mice but not p75NTREXONIII knockout mice, indicating the antibodies are directed against the ligand binding extracellular region absent in knockout mice. Both MLR1 and MLR2 partially blocked NGF induced cell death in a mouse cell-line that expresses p75NTR but not TrKA. Importantly, intracerebroventricular injections indicated MLR2 was internalized within the cell bodies of mouse basal forebrain neurons, further demonstrating that this antibody is biologically active.
|MOUSE ANTI-NERVE GROWTH FACTOR RECEPTOR MONOCLONAL ANTIBODY|