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Anti-CDX-2, Clone CDX2-88 antibody

RRID:AB_2650531

Antibody ID

AB_2650531

Target Antigen

CDX-2

Proper Citation

(BioGenex Cat# AM392, RRID:AB_2650531)

Clonality

monoclonal antibody

Comments

A Balb/c mouse was immunized with a full-length CDX2 recombinant protein. Stable hybridomas were produced by fusion of spleen cells with P2/0 myeloma cell.

Clone ID

CDX2-88

Host Organism

mouse

Vendor

BioGenex

Cat Num

AM392 also AM392-10M, AM392-5M, MU392A-UC, MU392A-5UC

Generation of a human CDX2 knock-in reporter iPSC line (MHHi007-A-1) to model human trophoblast differentiation.

  • Malysheva SV
  • Stem Cell Res
  • 2018 May 19

Literature context: RRID:AB_2650531 goat anti-GFP (goat polyclonal)


Abstract:

Caudal-type homeobox 2 (CDX2) transcription factor is an important marker for early trophoblast lineages and intestinal epithelium. Due to its nuclear expression the immunostaining and sorting of viable CDX2pos cells is not possible. In this paper we report the generation and describe key characteristics of a CDX2Venus knock-in reporter hiPSC-cell line (MHHi007-A-1) which can serve as an in vitro tool to study human trophoblast and intestinal differentiation.

Funding information:
  • Canadian Institutes of Health Research - (Canada)

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

  • Morgani SM
  • Elife
  • 2018 Feb 7

Literature context: anti-CDX2 BioGenex Cat# AM392, RRID:AB_2650531 1:200


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()

Generation of Mouse and Human Organoid-Forming Intestinal Progenitor Cells by Direct Lineage Reprogramming.

  • Miura S
  • Cell Stem Cell
  • 2017 Oct 5

Literature context: 77163Mouse anti-CDX2BioGenexCat#MU392A-UCMouse anti-CK8/18Leica Biosystem


Abstract:

Intestinal organoids hold great promise as a valuable tool for studying and treating intestinal diseases. The currently available sources of human intestinal organoids, tissue fragments or pluripotent stem cells, involve invasive procedures or complex differentiation protocols, respectively. Here, we show that a set of four transcription factors, Hnf4α, Foxa3, Gata6, and Cdx2, can directly reprogram mouse fibroblasts to acquire the identity of fetal intestine-derived progenitor cells (FIPCs). These induced FIPCs (iFIPCs) form spherical organoids that develop into adult-type budding organoids containing cells with intestinal stem cell properties. The resulting stem cells produce all intestinal epithelial cell lineages and undergo self-renewing cell divisions. After transplantation, the induced spherical and budding organoids can reconstitute colonic and intestinal epithelia, respectively. The same combination of four defined transcription factors can also induce human iFIPCs. This alternative approach for producing intestinal organoids may well facilitate application for disease analysis and therapy development.

Lineage Establishment and Progression within the Inner Cell Mass of the Mouse Blastocyst Requires FGFR1 and FGFR2.

  • Kang M
  • Dev. Cell
  • 2017 Jun 5

Literature context: U-392AUC; RRID:AB_2650531 Goat anti-


Abstract:

Fibroblast growth factor 4 (FGF4) is the key signal driving specification of primitive endoderm (PrE) versus pluripotent epiblast (EPI) within the inner cell mass (ICM) of the mouse blastocyst. To gain insight into the receptor(s) responding to FGF4 within ICM cells, we combined single-cell-resolution quantitative imaging with single-cell transcriptomics of wild-type and Fgf receptor (Fgfr) mutant embryos. Despite the PrE-specific expression of FGFR2, it is FGFR1, expressed by all ICM cells, that is critical for establishment of a PrE identity. Signaling through FGFR1 is also required to constrain levels of the pluripotency-associated factor NANOG in EPI cells. However, the activity of both receptors is required for lineage establishment within the ICM. Gene expression profiling of 534 single ICM cells identified distinct downstream targets associated with each receptor. These data lead us to propose a model whereby unique and additive activities of FGFR1 and FGFR2 within the ICM coordinate establishment of two distinct lineages.

Funding information:
  • NCI NIH HHS - P30 CA008748()
  • NIDDK NIH HHS - R01 DK084391()

Distinct Requirements for FGFR1 and FGFR2 in Primitive Endoderm Development and Exit from Pluripotency.

  • Molotkov A
  • Dev. Cell
  • 2017 Jun 5

Literature context: U392A-UC; RRID:AB_2650531 Rabbit mon


Abstract:

Activation of the FGF signaling pathway during preimplantation development of the mouse embryo is known to be essential for differentiation of the inner cell mass and the formation of the primitive endoderm (PrE). We now show using fluorescent reporter knockin lines that Fgfr1 is expressed in all cell populations of the blastocyst, while Fgfr2 expression becomes restricted to extraembryonic lineages, including the PrE. We further show that loss of both receptors prevents the development of the PrE and demonstrate that FGFR1 plays a more prominent role in this process than FGFR2. Finally, we document an essential role for FGFRs in embryonic stem cell (ESC) differentiation, with FGFR1 again having a greater influence than FGFR2 in ESC exit from the pluripotent state. Collectively, these results identify mechanisms through which FGF signaling regulates inner cell mass lineage restriction and cell commitment during preimplantation development.

Funding information:
  • NCI NIH HHS - P30 CA196521()
  • NIDCR NIH HHS - R01 DE022778()