Not exact matches
Varghese and her team showed that they could
control the
differentiation of human pluripotent stem
cells into functional osteoblasts — bone - building
cells — simply by adding the molecule adenosine to their growth medium.
Directly or indirectly, Holick points out, «the active form
of vitamin D
controls up to 200 different genes,» including ones responsible for
cell proliferation,
differentiation, and death.
Since Yamanaka's breakthrough, dozens
of groups have reported other ways
of reprogramming
cells as well as techniques to
control differentiation of stem
cells into neurons, cardiovascular
cells, and other tissues
of interest for regenerative medicine.
JAK1 is part
of a well - studied regulatory network
of proteins that is involved in the
control of cell growth,
differentiation, apoptosis, inflammation, and immune response.
There is no question that ability to generate glucose - responsive, human beta
cells through
controlled differentiation of stem
cells will accelerate the development
of new therapeutics.
«In normal conditions, the microenvironment is able to
control the proliferation,
differentiation and migration
of the hematopoietic stem
cell.
The pair discovered a swath
of cells in frog embryos that
controls early
cell differentiation.
In CRC 873, funded by the German Research Foundation, medical and biological scientists investigate the basic regulatory mechanisms that
control the self - renewal and
differentiation of stem
cells.
Many breast cancers are marked by a lack
of HOXA5 protein, a gene product known to
control cell differentiation and death, and lower levels
of the protein correspond to poorer outcomes for patients.
«We were able to show that a significant number
of these adenomas carry a mutation in a gene that is involved in
controlling cell proliferation and
differentiation,» Calebiro further explained.
In the case
of planarians, the gene egr - 4 seems to perform an early
control of cell proliferation as a response to amputation, and be involved later in the early
differentiation of brain during regeneration.
Researchers in Japan have shown that modified gold nanoparticles can be used to
control the
differentiation of stem
cells into bone.
«A better way to grow bone
cells: New method allows for more
control in the
differentiation of stem
cells into bone
cells.»
The authors uncover the cellular and molecular mechanisms, as well as the gene network regulated by Sox9 during the early steps
of skin tumor initiation and demonstrates that Sox9
controls the long term maintenance and expansion
of oncogene expressing
cells by promoting self - renewing division and inhibiting
differentiation.
Researchers at the Institute for Stem
Cell Therapy and Exploration
of Monogenic Diseases (I - Stem — Inserm / AFM / UEVE), in collaboration with CNRS and Paris Descartes University, have recently developed a new approach to better
control the
differentiation of human pluripotent stem
cells, and thus produce different populations
of motor neurons from these
cells in only 14 days.
This inefficiency is partly due to a poor understanding
of the molecular mechanisms
controlling the
differentiation of these
cells.
The microparticles could also provide better
control over the kinetics
of cell differentiation.
The
differentiation of stem
cells is largely
controlled by external cues, including morphogenic growth factors, in the three - dimensional environment that surrounds the
cells.
Previously, in the region that
controls the function
of the transcription factor that promotes
differentiation from ES
cells to a specific
cell type, bivalent modifications
of histones such as the accelerator and brake histone marks for transcription were thought to have coexisted.
Its first target was the regulatory network involved in
controlling the
differentiation of THP - 1
cells, a line
of human leukemia
cells used in laboratory experiments.
Song explained the structural knowledge
of DNMT3A will allow scientists to
control DNA methylation content, gene expression, and
cell differentiation — all
of which are linked to diseases and finding cures for them.
In turn, the niche
cells control the production and also the
differentiation of the blood stem
cells.
Finally, I will show how we have combined our results to generate a model
of hematopoietic
differentiation where specific transcription factors
control lineage regulatory regions; our model predicts many already known lineage -
controlling factors as well as finds new potential regulators
of hematopoietic
differentiation such as ATF3 in monocytes and Tcf7l2 and Runx2 in NK
cells.
Unexpected positive
control of NFκB and miR - 155 by DGKα and ζ ensures effector and memory CD8 + T
cell differentiation.
Interplay between FGF2 and BMP
controls the self - renewal, dormancy and
differentiation of rat neuralstem
cells
Initial studies demonstrated that ligation
of 4 - 1BB on T
cells could deliver costimulatory signals resulting in either increased proliferation or enhanced cytokine secretion and also
control clonal expansion and
differentiation of effector and memory T
cells.
Alpha tubulin is not suitable as a loading
control in adipose tissue as expression
of tubulin in adipose tissue is very low (Spiegelman and Farmer,
Cell, 1982, 29 (1): 53 - 60, «in
cells undergoing adipose
differentiation actin synthesis decreases by 90 %»).
Title: Interplay between FGF2 and BMP
controls the self - renewal, dormancy and
differentiation of rat neural stem
cells Authors: Sun Y, Hu J, Zhou L, Pollard SM, and Smith A Date: June 2011 Publication Details: J
Cell Sci, Jun 1 2011:124 (11); 1867 - 1877
Professor Kyurkchiev's group is currently developing a project on the
controlled differentiation of human induced pluripotent stem
cells into hematopoietic stem
cells and lymphoid
cells.
The morphological changes manifested in the
cell types linked to larger toepads exemplify
cell type
differentiation that must be
controlled by the physiology
of reproduction and properly timed nutrient - dependent reproductive sexual behavior, which probably occurs near the location
of the higher perches.
To evaluate whether ABL kinases might regulate the secretion
of osteoblast - derived RANKL or OPG leading to osteoclast
differentiation, we analyzed RANKL and OPG mRNA abundance in the murine osteoblast
cell line 7F2 in response to conditioned medium from
control and ABL1 / ABL2 knockdown breast cancer
cells.
This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma
cell lines by modulating
cell cycle arrest and apoptosis.26, 27 As a mechanism
of action, KMT2D mutations
of B - lymphoma
cells promote malignant outgrowth by perturbing methylation
of H3K4 that affect the JAK - STAT, Toll - like receptor, or B -
cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction
of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T -
cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development
of all hematopoietic lineages32 and regulates lymphoid
cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis
of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to
control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action
of chidamide and decitabine may interfere with the
differentiation and / or viability
of PTCL - NOS through a PU.1 - dependent gene expression program.
Research Interests: Molecular
control of cell fate from stemness to differentiated skeletal and neuronal
cell types; SOX transcription factors; skeletal malformation and degeneration diseases; intellectual disability and autism spectrum disorders; mouse genetic models; human pluripotent stem
cell differentiation models in vitro
The origins
of many
of these and other genes specific to animal processes such as
cell adhesion, and social
control of cell proliferation, death and
differentiation can be traced to genomic events (gene birth, subfamily expansions, intron gain / loss, and so on) that occurred in the lineage that led to the metazoan ancestor, after animals diverged from their unicellular «cousins».
The fellow will drive a new project focusing on molecular mechanisms
controlling the identity, self - renewal, and
differentiation potential
of skeletal stem
cells.
Areas
of research include biochemical and cellular mechanisms, muscle contractility and
cell motility, the genetic
control of cell growth and
differentiation, and tissue damage and regeneration.
The positioning
of the
cells controls their genetic program and their
differentiation into embryonic or extra-embryonic tissues.
Susan Amara, USA - «Regulation
of transporter function and trafficking by amphetamines, Structure - function relationships in excitatory amino acid transporters (EAATs), Modulation
of dopamine transporters (DAT) by GPCRs, Genetics and functional analyses
of human trace amine receptors» Tom I. Bonner, USA (Past Core Member)- Genomics, G protein coupled receptors Michel Bouvier, Canada - Molecular Pharmacology
of G protein - Coupled Receptors; Molecular mechanisms
controlling the selectivity and efficacy
of GPCR signalling Thomas Burris, USA - Nuclear Receptor Pharmacology and Drug Discovery William A. Catterall, USA (Past Core Member)- The Molecular Basis
of Electrical Excitability Steven Charlton, UK - Molecular Pharmacology and Drug Discovery Moses Chao, USA - Mechanisms
of Neurotophin Receptor Signaling Mark Coles, UK - Cellular
differentiation, human embryonic stem
cells, stromal
cells, haematopoietic stem
cells, organogenesis, lymphoid microenvironments, develomental immunology Steven L. Colletti, USA Graham L Collingridge, UK Philippe Delerive, France - Metabolic Research (diabetes, obesity, non-alcoholic fatty liver, cardio - vascular diseases, nuclear hormone receptor, GPCRs, kinases) Sir Colin T. Dollery, UK (Founder and Past Core Member) Richard M. Eglen, UK Stephen M. Foord, UK David Gloriam, Denmark - GPCRs, databases, computational drug design, orphan recetpors Gillian Gray, UK Debbie Hay, New Zealand - G protein - coupled receptors, peptide receptors, CGRP, Amylin, Adrenomedullin, Migraine, Diabetes / obesity Allyn C. Howlett, USA Franz Hofmann, Germany - Voltage dependent calcium channels and the positive inotropic effect
of beta adrenergic stimulation; cardiovascular function
of cGMP protein kinase Yu Huang, Hong Kong - Endothelial and Metabolic Dysfunction, and Novel Biomarkers in Diabetes, Hypertension, Dyslipidemia and Estrogen Deficiency, Endothelium - derived Contracting Factors in the Regulation
of Vascular Tone, Adipose Tissue Regulation
of Vascular Function in Obesity, Diabetes and Hypertension, Pharmacological Characterization
of New Anti-diabetic and Anti-hypertensive Drugs, Hypotensive and antioxidant Actions
of Biologically Active Components
of Traditional Chinese Herbs and Natural Plants including Polypehnols and Ginsenosides Adriaan P. IJzerman, The Netherlands - G protein - coupled receptors; allosteric modulation; binding kinetics Michael F Jarvis, USA - Purines and Purinergic Receptors and Voltage-gated ion channel (sodium and calcium) pharmacology Pain mechanisms Research Reproducibility Bong - Kiun Kaang, Korea - G protein - coupled receptors; Glutamate receptors; Neuropsychiatric disorders Eamonn Kelly, Prof, UK - Molecular Pharmacology
of G protein - coupled receptors, in particular opioid receptors, regulation
of GPCRs by kinasis and arrestins Terry Kenakin, USA - Drug receptor pharmacodynamics, receptor theory Janos Kiss, Hungary - Neurodegenerative disorders, Alzheimer's disease Stefan Knapp, Germany - Rational design
of highly selective inhibitors (so call chemical probes) targeting protein kinases as well as protein interaction inhibitors
of the bromodomain family Andrew Knight, UK Chris Langmead, Australia - Drug discovery, GPCRs, neuroscience and analytical pharmacology Vincent Laudet, France (Past Core Member)- Evolution
of the Nuclear Receptor / Ligand couple Margaret R. MacLean, UK - Serotonin, endothelin, estrogen, microRNAs and pulmonary hyperten Neil Marrion, UK - Calcium - activated potassium channels, neuronal excitability Fiona Marshall, UK - GPCR molecular pharmacology, structure and drug discovery Alistair Mathie, UK - Ion channel structure, function and regulation, pain and the nervous system Ian McGrath, UK - Adrenoceptors; autonomic transmission; vascular pharmacology Graeme Milligan, UK - Structure, function and regulation
of G protein - coupled receptors Richard Neubig, USA (Past Core Member)- G protein signaling; academic drug discovery Stefan Offermanns, Germany - G protein - coupled receptors, vascular / metabolic signaling Richard Olsen, USA - Structure and function
of GABA - A receptors; mode
of action
of GABAergic drugs including general anesthetics and ethanol Jean - Philippe Pin, France (Past Core Member)- GPCR - mGLuR - GABAB - structure function relationship - pharmacology - biophysics Helgi Schiöth, Sweden David Searls, USA - Bioinformatics Graeme Semple, USA - GPCR Medicinal Chemistry Patrick M. Sexton, Australia - G protein - coupled receptors Roland Staal, USA - Microglia and neuroinflammation in neuropathic pain and neurological disorders Bart Staels, France - Nuclear receptor signaling in metabolic and cardiovascular diseases Katerina Tiligada, Greece - Immunopharmacology, histamine, histamine receptors, hypersensitivity, drug allergy, inflammation Georg Terstappen, Germany - Drug discovery for neurodegenerative diseases with a focus on AD Mary Vore, USA - Activity and regulation
of expression and function
of the ATP - binding cassette (ABC) transporters
My recent studies have demonstrated that during tumor progression, TGFβ signaling
controls differentiation of CD39 + CD73 + myeloid
cells (MC).
Genes involved in DNA damage
control and inhibition
of DNA synthesis [49], in particular Atm, Chk1 and Chk2, are also highly expressed in ES
cells, but decline during
differentiation.
usage
of model organisms to understand and exploit the mechanisms
controlling stem and precursor
cell generation, maintenance, activation, recruitment, proliferation, homing and
differentiation,
The use
of embryonic stem
cells as therapeutics requires firm understanding
of the mechanisms that
control their proliferation and
differentiation.
This protein helps
control the growth and division (proliferation)
of cells, the process by which
cells mature to carry out specific functions (
differentiation),
cell movement (motility), and the self - destruction
of cells (apoptosis).