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Anti-E-CADHERIN Monoclonal Antibody, Unconjugated, Clone ECCD-2

RRID:AB_86571

Antibody ID

AB_86571

Target Antigen

E-CADHERIN human, mouse eccd-2 antibody has moderate cross-reactivity with human e-cadherin

Proper Citation

(Innovative Research Cat# 13-1900, RRID:AB_86571)

Clonality

monoclonal antibody

Comments

manufacturer recommendations: Blocking/Neutralize; Flow Cytometry; Immunofluorescence; Immunohistochemistry; Immunoprecipitation; Western Blot; Flow cytometry, IF, IHC(FFPE), IP, WB, Inhibition of E-cadherin-dependent cell-cell contact

Clone ID

Clone ECCD-2

Host Organism

rat

Vendor

Innovative Research

Cat Num

13-1900

Publications that use this research resource

Myoepithelial Cells of Submucosal Glands Can Function as Reserve Stem Cells to Regenerate Airways after Injury.

  • Tata A
  • Cell Stem Cell
  • 2018 May 3

Literature context:


Abstract:

Cells demonstrate plasticity following injury, but the extent of this phenomenon and the cellular mechanisms involved remain underexplored. Using single-cell RNA sequencing (scRNA-seq) and lineage tracing, we uncover that myoepithelial cells (MECs) of the submucosal glands (SMGs) proliferate and migrate to repopulate the airway surface epithelium (SE) in multiple injury models. Specifically, SMG-derived cells display multipotency and contribute to basal and luminal cell types of the SMGs and SE. Ex vivo expanded MECs have the potential to repopulate and differentiate into SE cells when grafted onto denuded airway scaffolds. Significantly, we find that SMG-like cells appear on the SE of both extra- and intra-lobular airways of large animal lungs following severe injury. We find that the transcription factor SOX9 is necessary for MEC plasticity in airway regeneration. Because SMGs are abundant and present deep within airways, they may serve as a reserve cell source for enhancing human airway regeneration.

Funding information:
  • NHLBI NIH HHS - R00 HL127181()
  • NIDDK NIH HHS - DK59630(United States)
  • NIEHS NIH HHS - U01 ES017219()

YAP/TAZ-Dependent Reprogramming of Colonic Epithelium Links ECM Remodeling to Tissue Regeneration.

  • Yui S
  • Cell Stem Cell
  • 2018 Jan 4

Literature context:


Abstract:

Tissue regeneration requires dynamic cellular adaptation to the wound environment. It is currently unclear how this is orchestrated at the cellular level and how cell fate is affected by severe tissue damage. Here we dissect cell fate transitions during colonic regeneration in a mouse dextran sulfate sodium (DSS) colitis model, and we demonstrate that the epithelium is transiently reprogrammed into a primitive state. This is characterized by de novo expression of fetal markers as well as suppression of markers for adult stem and differentiated cells. The fate change is orchestrated by remodeling the extracellular matrix (ECM), increased FAK/Src signaling, and ultimately YAP/TAZ activation. In a defined cell culture system recapitulating the extracellular matrix remodeling observed in vivo, we show that a collagen 3D matrix supplemented with Wnt ligands is sufficient to sustain endogenous YAP/TAZ and induce conversion of cell fate. This provides a simple model for tissue regeneration, implicating cellular reprogramming as an essential element.

Funding information:
  • NCI NIH HHS - R01 CA084197-11(United States)