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Human/Mouse Brachyury Affinity Purified Polyclonal Ab antibody

RRID:AB_2200235

Antibody ID

AB_2200235

Target Antigen

Human/Mouse Brachyury Affinity Purified Ab human/mouse, human, mouse

Proper Citation

(R and D Systems Cat# AF2085, RRID:AB_2200235)

Clonality

polyclonal antibody

Comments

vendor recommendations: IgG Chromatin Immunoprecipitation (ChIP), Immunocytochemistry, Immunohistochemistry, Western Blot; Immunohistochemistry; Immunocytochemistry; Western Blot

Host Organism

goat

Vendor

R and D Systems

Generation of RAB39B knockout isogenic human embryonic stem cell lines to model RAB39B-mediated Parkinson's disease.

  • Gao Y
  • Stem Cell Res
  • 2018 Mar 3

Literature context:


Abstract:

Mutations in RAB39B are a known cause of X-linked early onset Parkinson's disease. Isogenic human embryonic stem cell lines carrying two independent deletions of RAB39B were generated using CRISPR/Cas9 genome editing tool. The deletions were confirmed by PCR and direct sequence analysis in two edited stem cell lines. Both cell lines showed pluripotency and displayed a normal karyotype. Further, they were able to form embryoid bodies in vitro, and express markers indicative of differentiation to the three germ layers.

Funding information:
  • Cancer Research UK - (United Kingdom)

Generation of induced pluripotent stem cell (iPSC) line from a 21-year-old X-linked adrenoleukodystrophy (X-ALD) patient.

  • You YR
  • Stem Cell Res
  • 2018 Mar 19

Literature context:


Abstract:

X-linked Adrenoleukodystrophy (X-ALD) is a genetic disease that caused by mutations in adenosine triphosphate [ATP]-binding-cassette transporter superfamily D member 1 (ABCD1) gene. We generated an induced pluripotent stem cell (iPSC) line from a 21-year-old male X-ALD patient-derived fibroblasts by Sendai virus mediated reprogramming. Established iPSCs stably expanded while maintaining immunoreactivity for various pluripotency markers and alkaline phosphatase, as well as normal 44+XY karyotype. Under the differentiation condition, the cells gave rise to cells of three germ layers.

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

  • Morgani SM
  • Elife
  • 2018 Feb 7

Literature context:


Abstract:

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()

Lymphoblast-derived integration-free ISRM-CON9 iPS cell line from a 75year old female.

  • Martins S
  • Stem Cell Res
  • 2017 Dec 22

Literature context:


Abstract:

Human lymphoblast cells were used to generate integration-free induced pluripotent stem cells (iPSCs) employing episomal-based plasmids expressing OCT4, SOX2, NANOG, LIN28, c-MYC and L-MYC. The derived iPSCs were defined as pluripotent based on (i) expression of pluripotency-associated markers, (ii) embryoid body-based differentiation into cell types representative of the three germ layers and (iii) the similarity between the transcriptomes of the iPSC line and the human embryonic stem cell line H1 with a Pearson correlation of 0.95.

Zfp281 is essential for mouse epiblast maturation through transcriptional and epigenetic control of Nodal signaling.

  • Huang X
  • Elife
  • 2017 Nov 23

Literature context:


Abstract:

Pluripotency is defined by a cell's potential to differentiate into any somatic cell type. How pluripotency is transited during embryo implantation, followed by cell lineage specification and establishment of the basic body plan, is poorly understood. Here we report the transcription factor Zfp281 functions in the exit from naive pluripotency occurring coincident with pre-to-post-implantation mouse embryonic development. By characterizing Zfp281 mutant phenotypes and identifying Zfp281 gene targets and protein partners in developing embryos and cultured pluripotent stem cells, we establish critical roles for Zfp281 in activating components of the Nodal signaling pathway and lineage-specific genes. Mechanistically, Zfp281 cooperates with histone acetylation and methylation complexes at target gene enhancers and promoters to exert transcriptional activation and repression, as well as epigenetic control of epiblast maturation leading up to anterior-posterior axis specification. Our study provides a comprehensive molecular model for understanding pluripotent state progressions in vivo during mammalian embryonic development.

Funding information:
  • NIDA NIH HHS - K02 DA021863-01A1(United States)

A Gene Regulatory Network Balances Neural and Mesoderm Specification during Vertebrate Trunk Development.

  • Gouti M
  • Dev. Cell
  • 2017 May 8

Literature context:


Abstract:

Transcriptional networks, regulated by extracellular signals, control cell fate decisions and determine the size and composition of developing tissues. One example is the network controlling bipotent neuromesodermal progenitors (NMPs) that fuel embryo elongation by generating spinal cord and trunk mesoderm tissue. Here, we use single-cell transcriptomics to identify the molecular signature of NMPs and reverse engineer the mechanism that regulates their differentiation. Together with genetic perturbations, this reveals a transcriptional network that integrates opposing retinoic acid (RA) and Wnt signals to determine the rate at which cells enter and exit the NMP state. RA, produced by newly generated mesodermal cells, provides feedback that initiates NMP generation and induces neural differentiation, thereby coordinating the production of neural and mesodermal tissue. Together, the data define a regulatory network architecture that balances the generation of different cell types from bipotential progenitors in order to facilitate orderly axis elongation.

An Hdac1/Rpd3-Poised Circuit Balances Continual Self-Renewal and Rapid Restriction of Developmental Potential during Asymmetric Stem Cell Division.

  • Janssens DH
  • Dev. Cell
  • 2017 Feb 27

Literature context:


Abstract:

How the developmental potential of differentiating stem cell progeny becomes rapidly and stably restricted following asymmetric stem cell division is unclear. In the fly larval brain, earmuff (erm) uniquely functions to restrict the developmental potential of intermediate neural progenitors (INPs) generated by asymmetrically dividing neural stem cells (neuroblasts). Here we demonstrate that the histone deacetylase Hdac1/Rpd3 functions together with self-renewal transcriptional repressors to maintain the erm immature INP enhancer in an inactive but poised state in neuroblasts. Within 2 hr of immature INP birth, downregulation of repressor activities alleviates Rpd3-mediated repression on the erm enhancer, enabling acetylation of multiple histone proteins and activating Erm expression. Erm restricts the developmental potential in immature INPs by repressing genes encoding neuroblast transcriptional activators. We propose that poising the fast-activating enhancers of master regulators of differentiation through continual histone deacetylation in stem cells enables self-renewal and rapid restriction of developmental potential following asymmetric division.

Funding information:
  • NIGMS NIH HHS - R01 GM092818()
  • NIGMS NIH HHS - R01 GM111694()
  • NIGMS NIH HHS - T32 GM007315()
  • NINDS NIH HHS - R01 NS077914()

Assessing the bipotency of in vitro-derived neuromesodermal progenitors.

  • Tsakiridis A
  • F1000Res
  • 2015 Sep 28

Literature context:


Abstract:

Retrospective clonal analysis in the mouse has demonstrated that the posterior spinal cord neurectoderm and paraxial mesoderm share a common bipotent progenitor. These neuromesodermal progenitors (NMPs) are the source of new axial structures during embryonic rostrocaudal axis elongation and are marked by the simultaneous co-expression of the transcription factors T(Brachyury) (T(Bra)) and Sox2. NMP-like cells have recently been derived from pluripotent stem cells in vitro following combined stimulation of Wnt and fibroblast growth factor (FGF) signaling. Under these conditions the majority of cultures consist of T(Bra)/Sox2 co-expressing cells after 48-72 hours of differentiation. Although the capacity of these cells to generate posterior neural and paraxial mesoderm derivatives has been demonstrated at the population level, it is unknown whether a single in vitro-derived NMP can give rise to both neural and mesodermal cells. Here we demonstrate that T(Bra) positive cells obtained from mouse epiblast stem cells (EpiSCs) after culture in NMP-inducing conditions can generate both neural and mesodermal clones. This finding suggests that, similar to their embryonic counterparts, in vitro-derived NMPs are truly bipotent and can thus be exploited as a model for studying the molecular basis of developmental cell fate decisions.

Funding information:
  • Medical Research Council - MR/K011200/1()
  • Medical Research Council - MR/L012766/1()