Michael L. Robinson

ORCID: 0000-0003-4779-3426
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About
Contact & Profiles
Research Areas
  • Connexins and lens biology
  • Urological Disorders and Treatments
  • Fibroblast Growth Factor Research
  • Intraocular Surgery and Lenses
  • Wnt/β-catenin signaling in development and cancer
  • Corneal Surgery and Treatments
  • Retinal Development and Disorders
  • Aldose Reductase and Taurine
  • Epigenetics and DNA Methylation
  • Cancer Cells and Metastasis
  • Cancer-related Molecular Pathways
  • Renal and related cancers
  • Connective tissue disorders research
  • CRISPR and Genetic Engineering
  • Cancer-related gene regulation
  • Photoreceptor and optogenetics research
  • Neuroblastoma Research and Treatments
  • Neuroscience and Neural Engineering
  • PI3K/AKT/mTOR signaling in cancer
  • Cancer-related molecular mechanisms research
  • Extracellular vesicles in disease
  • Animal Genetics and Reproduction
  • Ocular Surface and Contact Lens
  • Neonatal Respiratory Health Research
  • Ocular Disorders and Treatments

Miami University
2014-2024

Saint Vincent College
2024

Pennsylvania State University
2024

University of Miami
2007-2021

Newcastle University
2019

Robinson Memorial Hospital
2018

University of Maryland, College Park
2016

Park University
2016

Stony Brook University
2013

Nationwide Children's Hospital
1998-2009

Fibroblast growth factor-23 (FGF23) is a phosphaturic hormone that contributes to several hypophosphatemic disorders by reducing the expression of type II sodium-phosphate cotransporters (NaPi-2a and NaPi-2c) in kidney proximal tubule serum 1,25-dihydroxyvitamin D 3 [1,25(OH) 2 ] levels. The FGF receptor(s) mediating action FGF23 vivo have remained elusive. In this study, we show tubules express FGFR1, −3, −4 but not FGFR2 mRNA. To determine which these three FGFRs mediates FGF23's actions,...

10.1152/ajprenal.90742.2008 article EN AJP Renal Physiology 2009-06-11

Abstract We developed stromal- and epithelial-specific cre-transgenic mice to directly visualize epithelial-mesenchymal transition (EMT) during cancer progression in vivo. Using three different oncogene-driven mouse mammary tumor models cell-fate mapping strategies, we show vivo evidence for the existence of EMT breast that myc can specifically elicit this process. Hierarchical cluster analysis genome-wide loss heterozygosity reveals incidence invasive human carcinomas is rare, but when it...

10.1158/0008-5472.can-07-2148 article EN Cancer Research 2008-02-01

Inflammation likely has a role in the early genesis of certain malignancies. Interleukin (IL)-15, proinflammatory cytokine and growth factor, is required for lymphocyte homeostasis. Intriguingly, expression IL-15 protein tightly controlled by multiple posttranscriptional mechanisms. Here, we engineered transgenic mouse to overexpress eliminating these checkpoints. mice have expansions natural killer (NK) CD8+ T lymphocytes. Later, develop fatal lymphocytic leukemia with T-NK phenotype. These...

10.1084/jem.193.2.219 article EN The Journal of Experimental Medicine 2001-01-15

Chlamydomonas reinhardtii hydin is a central pair protein required for flagellar motility, and mice with Hydin defects develop lethal hydrocephalus. To determine if in cause hydrocephalus through mechanism involving cilia, we compared the morphology, ultrastructure, activity of cilia wild-type mutant strains. The length density brains animals normal. ciliary axoneme normal respect to 9 + 2 microtubules, dynein arms, radial spokes but one two microtubules lacks specific projection. are unable...

10.1083/jcb.200710162 article EN The Journal of Cell Biology 2008-02-04

ABSTRACT The vertebrate ocular lens undergoes a spatially defined pattern of differentiation which may be regulated by the distribution proteins from fibroblast growth factor (FGF) family. ability altered FGF-1 (acidic FGF) to disrupt normal was evaluated production transgenic mice express under control lens-specific αA-crystallin promoter. Since lacks classical signal peptide consensus sequence, were also produced with chimeric construct containing sequence FGF-4 gene fused in frame coding...

10.1242/dev.121.2.505 article EN Development 1995-02-01

The lens of the eye is composed fiber cells, which differentiate from epithelial cells and undergo programmed organelle degradation during terminal differentiation. Although autophagy, a major intracellular system, constitutively active in these its physiological role has remained unclear. We have previously shown that Atg5-dependent macroautophagy not necessary for degradation, at least embryonic period. Here, we generated lens-specific Atg5 knock-out mice showed required any period life....

10.1074/jbc.m112.437103 article EN cc-by Journal of Biological Chemistry 2013-03-12

ABSTRACT Ocular lens development entails epithelial to fiber cell differentiation, defects in which cause congenital cataracts. We report the first single-cell multiomic atlas of development, leveraging snRNA-seq, snATAC-seq and CUT&RUN-seq discover previously unreported mechanisms fate determination cataract-linked regulatory networks. A comprehensive profile cis- trans-regulatory interactions, including for transcription factor MAF, is established across a temporal trajectory...

10.1242/dev.202249 article EN cc-by Development 2024-01-01

ABSTRACT Members of the fibroblast growth factor (FGF) family are thought to initiate biological responses through activation cell surface receptors which must dimerize transmit an intracellular signal. Mammalian lens epithelial cells respond exogenous extracellular FGF, either in tissue culture or transgenic mice, by initiating fiber differentiation. The role FGF signalling normal development was evaluated lens-specific synthesis a kinase-deficient receptor type I (FGFR1) mice. This...

10.1242/dev.121.12.3959 article EN Development 1995-12-01

We have investigated the role of Bmp signaling in development mouse lens using three experimental strategies. First, we shown that ligand inhibitor noggin can suppress differentiation primary fiber cells explant culture. Second, expressed a dominant-negative form type 1 family receptor Alk6 (Bmpr1b – Mouse Genome Informatics) transgenic mice and an inhibition cell be detected at E13.5. Interestingly, observed was asymmetrical appeared only on nasal side ventral half. Expression inhibitory...

10.1242/dev.129.15.3727 article EN Development 2002-08-01

Retinoblastoma (Rb)-deficient embryos show severe defects in neurogenesis, erythropoiesis, and lens development die at embryonic day 14.5. Our recent results demonstrated a drastic disorganization of the labyrinth layer placenta Rb-deficient embryos, accompanied by reduced placental transport function. When these Rb-/- were supplied with wild-type using either tetraploid aggregation or genetic approaches, animals survived until birth. Here we analyze role extraembryonic Rb regulating...

10.1073/pnas.1031853100 article EN Proceedings of the National Academy of Sciences 2003-05-05

Apoptosis is an essential process during normal neuronal development. Approximately one-half of the neurons produced neurogenesis die before completion CNS maturation. To characterize role inhibitor apoptosis gene, survivin , neurogenesis, we used Cre -loxP -system to generate mice lacking in precursor cells. Conditional deletion starting at embryonic day 10.5 leads massive cells CNS. mutants were born expected Mendelian ratios; however, these died shortly after birth from respiratory...

10.1523/jneurosci.1446-05.2005 article EN cc-by-nc-sa Journal of Neuroscience 2005-07-27

The developing ocular lens provides an excellent model system with which to study the intrinsic and extrinsic cues governing cell differentiation. Although transcription factors Pax6 Sox2 have been shown be essential for induction, their later roles during fiber differentiation remain largely unknown. Using Cre/loxP mutagenesis, we somatically inactivated in mouse of secondary fibers explored regulatory interactions these two canonical Wnt pathway. Analysis Pax6-deficient lenses revealed a...

10.1242/dev.032888 article EN Development 2009-07-02
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