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Nanog Monoclonal Antibody (eBioMLC-51), eBioscience(TM)


Antibody ID


Target Antigen

Nanog See NCBI gene mouse

Proper Citation

(Thermo Fisher Scientific Cat# 14-5761-80, RRID:AB_763613)


monoclonal antibody


Applications: WB (2 µg/mL), ICC (2 µg/mL), IF (2 µg/mL)

Clone ID

Clone eBioMLC-51

Host Organism



Thermo Fisher Scientific Go To Vendor

Cat Num


Publications that use this research resource

Exit from Naive Pluripotency Induces a Transient X Chromosome Inactivation-like State in Males.

  • Sousa EJ
  • Cell Stem Cell
  • 2018 Jun 1

Literature context: her Scientific Cat# 14-5761-80, RRID:AB_763613 Monoclonal rabbit anti-Oct4 Cel


A hallmark of naive pluripotency is the presence of two active X chromosomes in females. It is not clear whether prevention of X chromosome inactivation (XCI) is mediated by gene networks that preserve the naive state. Here, we show that robust naive pluripotent stem cell (nPSC) self-renewal represses expression of Xist, the master regulator of XCI. We found that nPSCs accumulate Xist on the male X chromosome and on both female X chromosomes as they become NANOG negative at the onset of differentiation. This is accompanied by the appearance of a repressive chromatin signature and partial X-linked gene silencing, suggesting a transient and rapid XCI-like state in male nPSCs. In the embryo, Xist is transiently expressed in males and in females from both X chromosomes at the onset of naive epiblast differentiation. In conclusion, we propose that XCI initiation is gender independent and triggered by destabilization of naive identity, suggesting that gender-specific mechanisms follow, rather than precede, XCI initiation.

Funding information:
  • NHLBI NIH HHS - HL085036(United States)

Esrrb Unlocks Silenced Enhancers for Reprogramming to Naive Pluripotency.

  • Adachi K
  • Cell Stem Cell
  • 2018 Jun 11

Literature context: her Scientific Cat# 14-5761-80; RRID:AB_763613 Rabbit polyclonal anti-mKO2 MBL


Transcription factor (TF)-mediated reprogramming to pluripotency is a slow and inefficient process, because most pluripotency TFs fail to access relevant target sites in a refractory chromatin environment. It is still unclear how TFs actually orchestrate the opening of repressive chromatin during the long latency period of reprogramming. Here, we show that the orphan nuclear receptor Esrrb plays a pioneering role in recruiting the core pluripotency factors Oct4, Sox2, and Nanog to inactive enhancers in closed chromatin during the reprogramming of epiblast stem cells. Esrrb binds to silenced enhancers containing stable nucleosomes and hypermethylated DNA, which are inaccessible to the core factors. Esrrb binding is accompanied by local loss of DNA methylation, LIF-dependent engagement of p300, and nucleosome displacement, leading to the recruitment of core factors within approximately 2 days. These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.

Funding information:
  • Intramural NIH HHS - Z01 AI000904-06(United States)

Micropattern differentiation of mouse pluripotent stem cells recapitulates embryo regionalized cell fate patterning.

  • Morgani SM
  • Elife
  • 2018 Feb 7

Literature context: her Scientific Cat# 14-5761-80, RRID:AB_763613 1:200


During gastrulation epiblast cells exit pluripotency as they specify and spatially arrange the three germ layers of the embryo. Similarly, human pluripotent stem cells (PSCs) undergo spatially organized fate specification on micropatterned surfaces. Since in vivo validation is not possible for the human, we developed a mouse PSC micropattern system and, with direct comparisons to mouse embryos, reveal the robust specification of distinct regional identities. BMP, WNT, ACTIVIN and FGF directed mouse epiblast-like cells to undergo an epithelial-to-mesenchymal transition and radially pattern posterior mesoderm fates. Conversely, WNT, ACTIVIN and FGF patterned anterior identities, including definitive endoderm. By contrast, epiblast stem cells, a developmentally advanced state, only specified anterior identities, but without patterning. The mouse micropattern system offers a robust scalable method to generate regionalized cell types present in vivo, resolve how signals promote distinct identities and generate patterns, and compare mechanisms operating in vivo and in vitro and across species.

Funding information:
  • Cancer Research UK - 06-914/915(United Kingdom)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development - R01HD080699()
  • National Cancer Institute - P30CA008748()
  • National Institute of Diabetes and Digestive and Kidney Diseases - R01DK084391()
  • National Science Foundation - PHY1502151()
  • NYSTEM - C029568()

A lncRNA fine tunes the dynamics of a cell state transition involving Lin28, let-7 and de novo DNA methylation.

  • Li MA
  • Elife
  • 2017 Aug 18

Literature context: re Nanog (eBioscience, 14-5761, RRID:AB_763613, 1:200) and Lin28a (Cell signal


Execution of pluripotency requires progression from the naïve status represented by mouse embryonic stem cells (ESCs) to a state capacitated for lineage specification. This transition is coordinated at multiple levels. Non-coding RNAs may contribute to this regulatory orchestra. We identified a rodent-specific long non-coding RNA (lncRNA) linc1281, hereafter Ephemeron (Eprn), that modulates the dynamics of exit from naïve pluripotency. Eprn deletion delays the extinction of ESC identity, an effect associated with perduring Nanog expression. In the absence of Eprn, Lin28a expression is reduced which results in persistence of let-7 microRNAs, and the up-regulation of de novo methyltransferases Dnmt3a/b is delayed. Dnmt3a/b deletion retards ES cell transition, correlating with delayed Nanog promoter methylation and phenocopying loss of Eprn or Lin28a. The connection from lncRNA to miRNA and DNA methylation facilitates the acute extinction of naïve pluripotency, a pre-requisite for rapid progression from preimplantation epiblast to gastrulation in rodents. Eprn illustrates how lncRNAs may introduce species-specific network modulations.

Funding information:
  • NCI NIH HHS - R01 CA139067()
  • NCI NIH HHS - R21 CA175560()
  • Wellcome Trust - P01 CA013106()

An Interaction Landscape of Ubiquitin Signaling.

  • Zhang X
  • Mol. Cell
  • 2017 Mar 2

Literature context: 4-5761-80 RRID:AB_763613 Nestin BD


Intracellular signaling via the covalent attachment of different ubiquitin linkages to protein substrates is fundamental to many cellular processes. Although linkage-selective ubiquitin interactors have been studied on a case-by-case basis, proteome-wide analyses have not been conducted yet. Here, we present ubiquitin interactor affinity enrichment-mass spectrometry (UbIA-MS), a quantitative interaction proteomics method that makes use of chemically synthesized diubiquitin to enrich and identify ubiquitin linkage interactors from crude cell lysates. UbIA-MS reveals linkage-selective diubiquitin interactions in multiple cell types. For example, we identify TAB2 and TAB3 as novel K6 diubiquitin interactors and characterize UCHL3 as a K27-linkage selective interactor that regulates K27 polyubiquitin chain formation in cells. Additionally, we show a class of monoubiquitin and K6 diubiquitin interactors whose binding is induced by DNA damage. We expect that our proteome-wide diubiquitin interaction landscape and established workflows will have broad applications in the ongoing efforts to decipher the complex language of ubiquitin signaling.