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Fab fragment Unconjugated Donkey Anti-Mouse IgG (H+L) Lot87807 antibody

RRID:AB_2307338

Antibody ID

AB_2307338

Target Antigen

Fab fragment Unconjugated Donkey Anti-Mouse IgG (H+L) null

Proper Citation

(Jackson ImmunoResearch Labs Cat# 715-007-003, RRID:AB_2307338)

Clonality

polyclonal antibody

Comments

Fab fragment Unconjugated Donkey Anti-Mouse IgG (H+L)

Host Organism

donkey

Vendor

Jackson ImmunoResearch Labs Go To Vendor

Cat Num

715-007-003

Publications that use this research resource

The cellular prion protein promotes olfactory sensory neuron survival and axon targeting during adult neurogenesis.

  • Parrie LE
  • Dev. Biol.
  • 2018 Jun 1

Literature context:


Abstract:

The cellular prion protein (PrPC) has been associated with diverse biological processes including cell signaling, neurogenesis, and neuroprotection, but its physiological function(s) remain ambiguous. Here we determine the role of PrPC in adult neurogenesis using the olfactory system model in transgenic mice. Olfactory sensory neurons (OSNs) within the olfactory sensory epithelium (OSE) undergo neurogenesis, integration, and turnover even into adulthood. The neurogenic processes of proliferation, differentiation/maturation, and axon targeting were evaluated in wild type, PrP-overexpressing, and PrP-null transgenic mice. Our results indicate that PrPC plays a role in maintaining mature OSNs within the epithelium: overexpression of PrPC resulted in greater survival of mitotically active cells within the OSE, whereas absence of prion protein resulted in fewer cells being maintained over time. These results are supported by both quantitative PCR analysis of gene expression and protein analysis characteristic of OSN differentiation. Finally, evaluation of axon migration determined that OSN axon targeting in the olfactory bulb is PrPC dose-dependent. Together, these findings provide new mechanistic insight into the neuroprotective role for PrPC in adult OSE neurogenesis, whereby more mature neurons are stably maintained in animals expressing PrPC.

Funding information:
  • NIAID NIH HHS - AI81789(United States)
  • NINDS NIH HHS - R21 NS096662(United States)

Radial Glial Fibers Promote Neuronal Migration and Functional Recovery after Neonatal Brain Injury.

  • Jinnou H
  • Cell Stem Cell
  • 2018 Jan 4

Literature context:


Abstract:

Radial glia (RG) are embryonic neural stem cells (NSCs) that produce neuroblasts and provide fibers that act as a scaffold for neuroblast migration during embryonic development. Although they normally disappear soon after birth, here we found that RG fibers can persist in injured neonatal mouse brains and act as a scaffold for postnatal ventricular-subventricular zone (V-SVZ)-derived neuroblasts that migrate to the lesion site. This injury-induced maintenance of RG fibers has a limited time window during post-natal development and promotes directional saltatory movement of neuroblasts via N-cadherin-mediated cell-cell contacts that promote RhoA activation. Transplanting an N-cadherin-containing scaffold into injured neonatal brains likewise promotes migration and maturation of V-SVZ-derived neuroblasts, leading to functional improvements in impaired gait behaviors. Together these results suggest that RG fibers enable postnatal V-SVZ-derived neuroblasts to migrate toward sites of injury, thereby enhancing neuronal regeneration and functional recovery from neonatal brain injuries.

Funding information:
  • NIDDK NIH HHS - R01 DK082659(United States)

Phosphorylation of NEUROG3 Links Endocrine Differentiation to the Cell Cycle in Pancreatic Progenitors.

  • Krentz NAJ
  • Dev. Cell
  • 2017 Apr 24

Literature context:


Abstract:

During pancreatic development, proliferating pancreatic progenitors activate the proendocrine transcription factor neurogenin 3 (NEUROG3), exit the cell cycle, and differentiate into islet cells. The mechanisms that direct robust NEUROG3 expression within a subset of progenitor cells control the size of the endocrine population. Here we demonstrate that NEUROG3 is phosphorylated within the nucleus on serine 183, which catalyzes its hyperphosphorylation and proteosomal degradation. During progression through the progenitor cell cycle, NEUROG3 phosphorylation is driven by the actions of cyclin-dependent kinases 2 and 4/6 at G1/S cell-cycle checkpoint. Using models of mouse and human pancreas development, we show that lengthening of the G1 phase of the pancreatic progenitor cell cycle is essential for proper induction of NEUROG3 and initiation of endocrine cell differentiation. In sum, these studies demonstrate that progenitor cell-cycle G1 lengthening, through its actions on stabilization of NEUROG3, is an essential variable in normal endocrine cell genesis.

Funding information:
  • NIDDK NIH HHS - P30 DK063720()
  • NIDDK NIH HHS - R01 DK021344()
  • NIDDK NIH HHS - U01 DK089541()