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Rat Anti-Mouse Uvomorulin/E-Cadherin Monoclonal Antibody, Unconjugated, Clone DECMA-1

RRID:AB_477600

Antibody ID

AB_477600

Target Antigen

Uvomorulin / E-Cadherin bovine, canine, human, mouse, human, bovine, canine, mouse

Proper Citation

(Sigma-Aldrich Cat# U3254, RRID:AB_477600)

Clonality

monoclonal antibody

Comments

Vendor recommendations: Functional Assay; Immunofluorescence; Immunohistochemistry; Immunoprecipitation; Western Blot; Indirect Immunofluorescence, Immunohistochemistry (Frozen sections), Immunoprecipitation, Western Blot, Functional assay

Clone ID

Clone DECMA-1

Host Organism

rat

Vendor

Sigma-Aldrich

Cat Num

U3254

Helicobacter pylori Infection Modulates Host Cell Metabolism through VacA-Dependent Inhibition of mTORC1.

  • Kim IJ
  • Cell Host Microbe
  • 2018 May 9

Literature context:


Abstract:

Helicobacter pylori (Hp) vacuolating cytotoxin (VacA) is a bacterial exotoxin that enters host cells and induces mitochondrial dysfunction. However, the extent to which VacA-dependent mitochondrial perturbations affect overall cellular metabolism is poorly understood. We report that VacA perturbations in mitochondria are linked to alterations in cellular amino acid homeostasis, which results in the inhibition of mammalian target of rapamycin complex 1 (mTORC1) and subsequent autophagy. mTORC1, which regulates cellular metabolism during nutrient stress, is inhibited during Hp infection by a VacA-dependent mechanism. This VacA-dependent inhibition of mTORC1 signaling is linked to the dissociation of mTORC1 from the lysosomal surface and results in activation of cellular autophagy through the Unc 51-like kinase 1 (Ulk1) complex. VacA intoxication results in reduced cellular amino acids, and bolstering amino acid pools prevents VacA-mediated mTORC1 inhibition. Overall, these studies support a model that Hp modulate host cell metabolism through the action of VacA at mitochondria.

Funding information:
  • NIAID NIH HHS - R01 AI045928()
  • NIAID NIH HHS - R21 AI117497()
  • NIAID NIH HHS - U19 AI106772(United States)
  • NIGMS NIH HHS - R01 GM089771()

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()

Crk proteins transduce FGF signaling to promote lens fiber cell elongation.

  • Collins TN
  • Elife
  • 2018 Jan 23

Literature context:


Abstract:

Specific cell shapes are fundamental to the organization and function of multicellular organisms. Fibroblast Growth Factor (FGF) signaling induces the elongation of lens fiber cells during vertebrate lens development. Nonetheless, exactly how this extracellular FGF signal is transmitted to the cytoskeletal network has previously not been determined. Here, we show that the Crk family of adaptor proteins, Crk and Crkl, are required for mouse lens morphogenesis but not differentiation. Genetic ablation and epistasis experiments demonstrated that Crk and Crkl play overlapping roles downstream of FGF signaling in order to regulate lens fiber cell elongation. Upon FGF stimulation, Crk proteins were found to interact with Frs2, Shp2 and Grb2. The loss of Crk proteins was partially compensated for by the activation of Ras and Rac signaling. These results reveal that Crk proteins are important partners of the Frs2/Shp2/Grb2 complex in mediating FGF signaling, specifically promoting cell shape changes.

Funding information:
  • National Eye Institute - 5P30EY019007()
  • National Eye Institute - EY017061()
  • NCI NIH HHS - R21-CA102733(United States)
  • NEI NIH HHS - R01 EY017061()
  • Research to Prevent Blindness - Jules and Doris Stein professorship()

Global expression profiling of globose basal cells and neurogenic progression within the olfactory epithelium.

  • Krolewski RC
  • J. Comp. Neurol.
  • 2013 Mar 1

Literature context:


Abstract:

Ongoing, lifelong neurogenesis maintains the neuronal population of the olfactory epithelium in the face of piecemeal neuronal turnover and restores it following wholesale loss. The molecular phenotypes corresponding to different stages along the progression from multipotent globose basal cell (GBC) progenitor to differentiated olfactory sensory neuron are poorly characterized. We used the transgenic expression of enhanced green fluorescent protein (eGFP) and cell surface markers to FACS-isolate ΔSox2-eGFP(+) GBCs, Neurog1-eGFP(+) GBCs and immature neurons, and ΔOMP-eGFP(+) mature neurons from normal adult mice. In addition, the latter two populations were also collected 3 weeks after olfactory bulb ablation, a lesion that results in persistently elevated neurogenesis. Global profiling of mRNA from the populations indicates that all stages of neurogenesis share a cohort of >2,100 genes that are upregulated compared to sustentacular cells. A further cohort of >1,200 genes are specifically upregulated in GBCs as compared to sustentacular cells and differentiated neurons. The increased rate of neurogenesis caused by olfactory bulbectomy had little effect on the transcriptional profile of the Neurog1-eGFP(+) population. In contrast, the abbreviated lifespan of ΔOMP-eGFP(+) neurons born in the absence of the bulb correlated with substantial differences in gene expression as compared to the mature neurons of the normal epithelium. Detailed examination of the specific genes upregulated in the different progenitor populations revealed that the chromatin modifying complex proteins LSD1 and coREST were expressed sequentially in upstream ΔSox2-eGFP(+) GBCs and Neurog1-eGFP(+) GBCs/immature neurons. The expression patterns of these proteins are dynamically regulated after activation of the epithelium by methyl bromide lesion.

Funding information:
  • NHLBI NIH HHS - U54-HL108460(United States)