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PAX6 antibody - Stem Cell Marker


Antibody ID


Target Antigen

PAX6 antibody - Stem Cell Marker mouse, human, sheep, non-human primate, rat, human, mouse, rat, rhesus monkey, sheep



Cat Num


Proper Citation

(Abcam Cat# ab5790, RRID:AB_305110)


polyclonal antibody

Host Organism



validation status unknown, seller recommendations provided in 2012: Flow Cyt, ICC/IF, IHC-Fr, IHC-P, WB; Immunofluorescence; Immunohistochemistry; Immunohistochemistry - frozen; Flow Cytometry; Western Blot; Immunohistochemistry - fixed; Immunocytochemistry

Publications that use this research resource

SETD7 Drives Cardiac Lineage Commitment through Stage-Specific Transcriptional Activation.

  • Lee J
  • Cell Stem Cell
  • 2018 Mar 1

Literature context: D:AB_444246Anti-PAX6Abcamab5790 RRID:AB_305110Anti-Alpha-1 fetoproteinDakoA000


Cardiac development requires coordinated and large-scale rearrangements of the epigenome. The roles and precise mechanisms through which specific epigenetic modifying enzymes control cardiac lineage specification, however, remain unclear. Here we show that the H3K4 methyltransferase SETD7 controls cardiac differentiation by reading H3K36 marks independently of its enzymatic activity. Through chromatin immunoprecipitation sequencing (ChIP-seq), we found that SETD7 targets distinct sets of genes to drive their stage-specific expression during cardiomyocyte differentiation. SETD7 associates with different co-factors at these stages, including SWI/SNF chromatin-remodeling factors during mesodermal formation and the transcription factor NKX2.5 in cardiac progenitors to drive their differentiation. Further analyses revealed that SETD7 binds methylated H3K36 in the bodies of its target genes to facilitate RNA polymerase II (Pol II)-dependent transcription. Moreover, abnormal SETD7 expression impairs functional attributes of terminally differentiated cardiomyocytes. Together, these results reveal how SETD7 acts at sequential steps in cardiac lineage commitment, and they provide insights into crosstalk between dynamic epigenetic marks and chromatin-modifying enzymes.

Funding information:
  • NCI NIH HHS - R01 CA124596(United States)
  • NHLBI NIH HHS - K99 HL133473()

Mild myelin disruption elicits early alteration in behavior and proliferation in the subventricular zone.

  • Gould EA
  • Elife
  • 2018 Feb 13

Literature context: m, ab5790, RRID:AB_305110), rat anti-PLP1 (clone AA3)(Yam


Myelin, the insulating sheath around axons, supports axon function. An important question is the impact of mild myelin disruption. In the absence of the myelin protein proteolipid protein (PLP1), myelin is generated but with age, axonal function/maintenance is disrupted. Axon disruption occurs in Plp1-null mice as early as 2 months in cortical projection neurons. High-volume cellular quantification techniques revealed a region-specific increase in oligodendrocyte density in the olfactory bulb and rostral corpus callosum that increased during adulthood. A distinct proliferative response of progenitor cells was observed in the subventricular zone (SVZ), while the number and proliferation of parenchymal oligodendrocyte progenitor cells was unchanged. This SVZ proliferative response occurred prior to evidence of axonal disruption. Thus, a novel SVZ response contributes to the region-specific increase in oligodendrocytes in Plp1-null mice. Young adult Plp1-null mice exhibited subtle but substantial behavioral alterations, indicative of an early impact of mild myelin disruption.

Funding information:
  • National Institutes of Health - AG053690()
  • National Institutes of Health - DC00566()
  • National Institutes of Health - DC012280()
  • National Institutes of Health - DC014253()
  • National Institutes of Health - NS099042()
  • National Institutes of Health - NS25304()
  • NCI NIH HHS - R33CA81671(United States)

Epigenetic Activation of WNT5A Drives Glioblastoma Stem Cell Differentiation and Invasive Growth.

  • Hu B
  • Cell
  • 2016 Nov 17

Literature context: t# ab5790 RRID:AB_305110 Rabbit mon


Glioblastoma stem cells (GSCs) are implicated in tumor neovascularization, invasiveness, and therapeutic resistance. To illuminate mechanisms governing these hallmark features, we developed a de novo glioblastoma multiforme (GBM) model derived from immortalized human neural stem/progenitor cells (hNSCs) to enable precise system-level comparisons of pre-malignant and oncogene-induced malignant states of NSCs. Integrated transcriptomic and epigenomic analyses uncovered a PAX6/DLX5 transcriptional program driving WNT5A-mediated GSC differentiation into endothelial-like cells (GdECs). GdECs recruit existing endothelial cells to promote peritumoral satellite lesions, which serve as a niche supporting the growth of invasive glioma cells away from the primary tumor. Clinical data reveal higher WNT5A and GdECs expression in peritumoral and recurrent GBMs relative to matched intratumoral and primary GBMs, respectively, supporting WNT5A-mediated GSC differentiation and invasive growth in disease recurrence. Thus, the PAX6/DLX5-WNT5A axis governs the diffuse spread of glioma cells throughout the brain parenchyma, contributing to the lethality of GBM.

Funding information:
  • NINDS NIH HHS - R56 NS094589(United States)

Neonatal disease environment limits the efficacy of retinal transplantation in the LCA8 mouse model.

  • Cho SH
  • BMC Ophthalmol
  • 2016 Nov 4

Literature context: I (Wako, 019-19741), anti-Pax6 (Abcam, ab5790), anti- phosphosynaptic density


BACKGROUND: Mutations of Crb1 gene cause irreversible and incurable visual impairment in humans. This study aims to use an LCA8-like mouse model to identify host-mediated responses that might interfere with survival, retinal integration and differentiation of grafted cells during neonatal cell therapy. METHODS: Mixed retinal donor cells (1 ~ 2 × 104) isolated from neural retinas of neonatal eGFP transgenic mice were injected into the subretinal space of LCA8-like model neonatal mice. Markers of specific cell types were used to analyze microglial attraction, CSPG induction and retinal cell differentiation. The positions of host retinal cells were traced according to their laminar location during disease progression to look for host cell rearrangements that might inhibit retinal integration of the transplanted cells. RESULTS: Transplanted retinal cells showed poor survival and attracted microglial cells, but CSPG was not greatly induced. Retinas of the LCA8 model hosts underwent significant cellular rearrangement, including rosette formation and apical displacement of inner retinal cells. CONCLUSIONS: Local disease environment, particularly host immune responses to injected cells and formation of a physical barrier caused by apical migration of host retinal cells upon disruption of outer limiting membrane, may impose two major barriers in LCAs cell transplantation therapy.

Funding information:
  • NINDS NIH HHS - R01 NS083726(United States)

Formation and maturation of parallel fiber-Purkinje cell synapses in the Staggerer cerebellum ex vivo.

  • Janmaat S
  • J. Comp. Neurol.
  • 2009 Feb 1

Literature context:


In vivo, homozygous staggerer (Rora(sg/sg)) Purkinje cells (PCs) remain in an early stage of development with rudimentary spineless dendrites, associated with a lack of parallel fiber (PF) input and the persistence of multiple climbing fibers (CFs). In this immunocytochemical study we used cerebellar organotypic cultures to monitor the development of Rora(sg/sg) PF-PC synapses in the absence of CF innervation. Ex vivo the vesicular glutamate transporters VGluT1 and VGluT2 reactivity was preferentially localized around the Rora(sg/sg) PC soma and proximal dendrites, which are typically CF domains. The shift from VGluT2 to VGluT1 in PF terminals during development was delayed in Rora(sg/sg) slices. The postsynaptic receptors mGluR1 and GluRdelta2 were differently distributed on Rora(sg/sg) PCs. mGluR1 reactivity was evenly distributed in PC soma and dendrites, whereas GluRdelta2 reactivity, normally restricted at PF synapses, was dense in Rora(sg/sg) PC somata. The presynaptic distribution of VGluT1 and VGluT2 on Rora(sg/sg) PCs matched the postsynaptic distribution of the glutamate receptor GluRdelta2, but not mGluR1.