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Nestin antibody [2Q178] - Neural Stem Cell Marker


Antibody ID


Target Antigen

Nestin human, mouse, rat

Proper Citation

(Abcam Cat# ab6142, RRID:AB_305313)


monoclonal antibody


validation status unknown, seller recommendations provided in 2012: Electron Microscopy; Immunocytochemistry; Immunohistochemistry; Western Blot; EM, Immunocytochemistry, Immunocytochemistry/Immunofluorescence, Immunohistochemistry-FoFr, Immunohistochemistry-Fr, Immunohistochemistry-P, Western Blot

Clone ID

Clone 2Q178

Host Organism




Cat Num


Publications that use this research resource

Transcriptional profiling of human neural precursors post alcohol exposure reveals impaired neurogenesis via dysregulation of ERK signaling and miR-145.

  • Louis LK
  • J. Neurochem.
  • 2017 Aug 21

Literature context:


Gestational alcohol exposure causes a range of neuropsychological disorders by modulating neurodevelopmental genes and proteins. The extent of damage depends on the stage of the embryo as well as dosage, duration and frequency of exposure. Here, we investigated the neurotoxic effects of alcohol using human embryonic stem cells. Multiple read-outs were engaged to assess the proliferation and differentiation capacity of neural precursor cells upon exposure to 100 mM ethanol for 48 h corresponding to the blood alcohol levels for binge drinkers. Whole-genome analysis revealed a spatiotemporal dysregulation of neuronal- and glial-specific gene expression that play critical roles in central nervous system (CNS) development. Alterations observed in the transcriptome may be attributed to epigenetic constitution witnessed by differential histone H3 Lys-4/Lys-27 modifications and acetylation status. In-depth mRNA and protein expression studies revealed abrogated extracellular signal-regulated kinases signaling in alcohol-treated cells. Consistent with this finding, ingenuity pathway analysis and micro-RNA profiling demonstrated up-regulation of miR-145 by targeting the neural specifier Sox-2. We also show that the neurite branching complexity of tubulin, beta 3 class III+ neurons was greatly reduced in response to alcohol. Finally, in vivo studies using zebrafish embryos reconfirmed the in vitro findings. Employing molecular endpoints in a human model, this report indicates for the first time that acute alcohol exposure could lead to impaired brain development via perturbation of extracellular signal-regulated kinases pathway and miR-145. However, it still needs to be addressed whether these modulations sustain throughout development, compromising the ability of the individual during adulthood and aging.

Funding information:
  • NCI NIH HHS - P50 CA070907(United States)

Lunatic fringe-mediated Notch signaling regulates adult hippocampal neural stem cell maintenance.

  • Semerci F
  • Elife
  • 2017 Jul 12

Literature context:


Hippocampal neural stem cells (NSCs) integrate inputs from multiple sources to balance quiescence and activation. Notch signaling plays a key role during this process. Here, we report that Lunatic fringe (Lfng), a key modifier of the Notch receptor, is selectively expressed in NSCs. Further, Lfng in NSCs and Notch ligands Delta1 and Jagged1, expressed by their progeny, together influence NSC recruitment, cell cycle duration, and terminal fate. We propose a new model in which Lfng-mediated Notch signaling enables direct communication between a NSC and its descendants, so that progeny can send feedback signals to the 'mother' cell to modify its cell cycle status. Lfng-mediated Notch signaling appears to be a key factor governing NSC quiescence, division, and fate.

Funding information:
  • NCI NIH HHS - P30 CA125123()
  • NCRR NIH HHS - S10 RR024574()
  • NIAID NIH HHS - P30 AI036211()
  • NICHD NIH HHS - U54 HD083092()
  • NIDCD NIH HHS - R01 DC006185()
  • NIDCD NIH HHS - R01 DC014832()
  • NIH HHS - S10 OD016167()

PCP4 (PEP19) overexpression induces premature neuronal differentiation associated with Ca(2+) /calmodulin-dependent kinase II-δ activation in mouse models of Down syndrome.

  • Mouton-Liger F
  • J. Comp. Neurol.
  • 2011 Oct 1

Literature context:


Pcp4/pep19 is a modulator of Ca(2+) -CaM, a key molecule for calcium signaling, expressed in postmitotic neuroectoderm cells during mouse embryogenesis. The PCP4 gene is located on human chromosome 21 and is present in three copies in Down syndrome (DS). To evaluate the consequences of three copies of this gene on the development of these cells in the nervous system, we constructed a transgenic (TgPCP4) mouse model, with one copy of human PCP4, and investigated the effects in this model and in the Ts1Cje, a mouse model of DS. During embryogenesis, we analyzed 1) the level of pcp4 transcript and protein in the two models; 2) the extent of colabeling for markers of neuronal differentiation (βIII-tubulin, Map2c, calbindin, and calretinin) and pcp4 by immunofluorescence analysis and overall protein levels of these markers by Western blotting; and 3) the rate of activation of CaMKII, a Ca(2+) -CaM target, to evaluate the impact of pcp4 overexpression on the Ca(2+) -CaM signaling pathway. We showed that three copies of the pcp4 gene induced the overexpression of transcripts and proteins during embryogenesis. Pcp4 overexpression 1) induced precocious neuronal differentiation, as shown by the distribution and levels of early neuronal markers; and 2) was associated with an increase in CaMKIIδ activation, confirming involvement in neuronal differentiation in vivo via a Pcp4-Ca(2+) -CaM pathway. TgPCP4 and Ts1Cje mice developed similar modifications, demonstrating that these mechanisms may account for abnormal neuronal development in DS.

Funding information:
  • NIDA NIH HHS - 1U54DA021519-01A1(United States)
  • NINDS NIH HHS - R01 NS36739(United States)