Ahlke Heydemann: Influence Statistics

Ahlke Heydemann

Ahlke Heydemann

Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, IL 60612, USA | Department of Physiology and Biophysics, University of Illinois at Chicago, ...

Ahlke Heydemann: Expert Impact

Concepts for which Ahlke Heydemann has direct influence: Muscular dystrophy , Skeletal muscle , Duchenne muscular dystrophy , Vascular spasm , Mouse models , Annexin a6 , Retinoic acid .

Ahlke Heydemann: KOL impact

Concepts related to the work of other authors for which for which Ahlke Heydemann has influence: Muscular dystrophy , Growth factor , Skeletal muscle , Fracture healing , Stem cells , Articular cartilage , Mdx mice .

KOL Resume for Ahlke Heydemann

Year
2021

Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, IL 60612, USA

2019

Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, IL, USA

2018

Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, IL 60612, USA;, ; Tel.: +1-312-355-0259; Fax: +1-312-996-1414

Center for Cardiovascular Research, The University of Illinois at Chicago, Chicago, IL 60612, USA

2017

University of Illinois at Chicago Department of Physiology and Biophysics Chicago Illinois USA

2016

Department of Physiology and Biophysics, The University of Illinois at Chicago, Chicago, IL 60612, USA.

The Center for Cardiovascular Research, Chicago, IL 60612, USA

2015

University of Illinois at Chicago Department of Physiology and Biophysics and Center for Cardiovascular Research Chicago Illinois USA

2014

Department of Physiology and Biophysics, University of Illinois, Chicago, IL 60612

Center for Cardiovascular Research, The University of Illinois at Chicago, Chicago, Illinois

2012

Department of Physiology and Biophysics, Center for Cardiovascular Research, The University of Illinois at Chicago, 60612, Chicago, IL, USA

2011

Department of Medicine, Sections of Cardiology, The University of Chicago

2010

Department of Medicine and

2009

Section of Cardiology, Department of Medicine, University of Chicago, 5841 S.Maryland, Chicago, IL 60637, USA.

2007

Department of Medicine, Section of Cardiology, The University of Chicago, Chicago, IL 60637, USA

2006

Department of Medicine, Section of Cardiology,

2005

Department of Medicine, The University of Chicago, Chicago, IL 60637, USA

2004

Department of Molecular Genetics and Cell Biology, Department of Medicine, and, Department of Human Genetics, The University of Chicago, Chicago, Illinois, USA.

2003

Department of Medicine, The University of Chicago, 5841 S. Maryland, MC6088 Chicago, IL, USA

2001

Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, IL, USA

2000

From the Departments of Molecular Genetics and Cell Biology and Medicine, and Howard Hughes Medical Institute, University of Chicago, Chicago, IL; and the Department of Molecular and Structural Biology, University of Aarhus, Aarhus, Denmark.

1997

Department of Medicine/Cardiology, University of Chicago, Chicago, Illinois, U.S.A.

1996

Department of Molecular Genetics and Cell Biology, University of Chicago, Illinois 60637, USA.

1994

Laboratory of Chemoprevention, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892

1992

Orthopaedic Research Unit, National Institute of Arthritis, Musculoskeletal, and Skin Diseases, National Institutes of Health, Bethesda, Maryland

1990

Orthopaedic Research Unit, NIAMS, NIH, Bethesda, Maryland, U.S.A

1989

the Laboratory of Developmental Biology and Anomalies, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892 USA

Prominent publications by Ahlke Heydemann

KOL-Index: 12467 . Chondrogenesis can occur during a bone repair process, which is related to several growth factors. Transforming growth factor beta 1 (TGF-beta 1) downregulates the expression of type II collagen by chondrocytes in vitro, but injection of TGF-beta 1 into the periosteum in vivo increases type II collagen mRNA levels and initiates chondrogenesis. We examined the effect of TGF-beta 1 on ...
Known for Growth Factor | Collagen Expression | Beta 1 | Alkaline Phosphatase
KOL-Index: 11766 . Pluripotent bone marrow-derived side population (BM-SP) stem cells have been shown to repopulate the hematopoietic system and to contribute to skeletal and cardiac muscle regeneration after transplantation. We tested BM-SP cells for their ability to regenerate heart and skeletal muscle using a model of cardiomyopathy and muscular dystrophy that lacks delta-sarcoglycan. The absence of ...
Known for Skeletal Muscle | Stem Cell | Situ Hybridization | Transplantation Hematopoietic
KOL-Index: 10455 . The protein product of the c-fps/fes (c-fes) proto-oncogene has been implicated in the normal development of myeloid cells (macrophages and neutrophils). mRNA for c-fes has been detected exclusively in myeloid cells and vascular endothelial cells in adult mammals. Although a 13-kilobase-pair (kb) human c-fes transgene exhibits high levels of expression in mice, the sequences that confer ...
Known for Fes Promoter | Myeloid Cells | Sp1 Transcription Factor | Proto Oncogene
KOL-Index: 10400 . RATIONALE: S100A12 is a small calcium binding protein that is a ligand of RAGE (receptor for advanced glycation end products). RAGE has been extensively implicated in inflammatory states such as atherosclerosis, but the role of S100A12 as its ligand is less clear. OBJECTIVE: To test the role of S100A12 in vascular inflammation, we generated and analyzed mice expressing human S100A12 in ...
Known for Aortic Aneurysm | S100a12 Mice | Transgenic Muscle | Vascular Smooth
KOL-Index: 10029 . Over the past decade different stem cell (SC) based approaches were tested to treat Duchenne Muscular Dystrophy (DMD), a lethal X-linked disorder caused by mutations in dystrophin gene. Despite research efforts, there is no curative therapy for DMD. Allogeneic SC therapies aim to restore dystrophin in the affected muscles; however, they are challenged by rejection and limited engraftment. ...
Known for Dystrophin Expressing | Chimeric Cells | Duchenne Muscular Dystrophy | Stem Cell
KOL-Index: 9984 . Most single-gene diseases, including muscular dystrophy, display a nonuniform phenotype. Phenotypic variability arises, in part, due to the presence of genetic modifiers that enhance or suppress the disease process. We employed an unbiased mapping approach to search for genes that modify muscular dystrophy in mice. In a genome-wide scan, we identified a single strong locus on chromosome 7 ...
Known for Muscular Dystrophy | Latent Tgf | Knockout Mice | Binding Protein
KOL-Index: 9317 . Loss-of-function mutations in the genes encoding dystrophin and the associated membrane proteins, the sarcoglycans, produce muscular dystrophy and cardiomyopathy. The dystrophin complex provides stability to the plasma membrane of striated muscle during muscle contraction. Increased SMAD signaling due to activation of the transforming growth factor-β (TGFβ) pathway has been described in ...
Known for Muscular Dystrophy | Smad Signaling | Muscle Dysfunction | Drosophila Model
KOL-Index: 9200 . Duchenne Muscular Dystrophy (DMD) is a progressive and lethal disease caused by mutations of the dystrophin gene. Currently no cure exists. Stem cell therapies targeting DMD are challenged by limited engraftment and rejection despite the use of immunosuppression. There is an urgent need to introduce new stem cell-based therapies that exhibit low allogenic profiles and improved cell ...
Known for Duchenne Muscular Dystrophy | Dystrophin Expressing Chimeric | Human Cells | Dec Dmd
KOL-Index: 8880 . Estrogen has profound effects on bone metabolism, yet its precise mechanism of action remains unknown. Several recent investigations have located the estrogen receptor (ER) on osteoblast-like cells, suggesting a potential direct action of estrogen via its own receptor on bone cells. The protective role of estrogen on bone in osteoporosis is well known; however, neither the existence nor ...
Known for Fracture Healing | Estrogen Receptor | Messenger Rats | Mrna Expression
KOL-Index: 8804 . Many monogenic disorders, including the muscular dystrophies, display phenotypic variability despite the same disease-causing mutation. To identify genetic modifiers of muscular dystrophy and its associated cardiomyopathy, we used quantitative trait locus mapping and whole genome sequencing in a mouse model. This approach uncovered a modifier locus on chromosome 11 associated with ...
Known for Muscular Dystrophy | Annexin A6 | Sarcolemmal Repair | Genetic Modifiers
KOL-Index: 8633 . Although transforming growth factors-beta and bone morphogenetic proteins are both capable of inducing bone formation in vivo, the target cells of their osteoinductive actions may be different. To evaluate periosteal cells as potential targets of the actions of transforming growth factor-beta and bone morphogenetic protein, we investigated the ability of three members of the transforming ...
Known for Transforming Growth | Collagen Gene | Factor Beta | Derived Cells
KOL-Index: 7606 . Duchenne Muscular Dystrophy (DMD) is a progressive lethal disease caused by X-linked mutations of the dystrophin gene. Dystrophin deficiency clinically manifests as skeletal and cardiac muscle weakness, leading to muscle wasting and premature death due to cardiac and respiratory failure. Currently, no cure exists. Since heart disease is becoming a leading cause of death in DMD patients, ...
Known for Duchenne Muscular Dystrophy | Dystrophin Expressing | Dec Cells | Mesenchymal Stem
KOL-Index: 7065 . BACKGROUND: The calcium-binding protein S100A12 is highly up-regulated in the serum and sputum of patients with allergic asthma and is suggested to be a biomarker and pathologic mediator of asthma. OBJECTIVE: To test the role of S100A12 in mediating airway inflammation in a mouse model of allergic lung inflammation. METHODS: Transgenic (TG) mice that express human S100A12 and wild-type ...
Known for Airway Inflammation | Transgenic Expression | Smooth Muscle | Human S100a12
KOL-Index: 6663 . Retinoic acid has been identified as a key morphogen governing pattern formation in the developing cartilaginous skeleton. Retinoids have also been implicated in the premature closure of the cartilage growth plate following vitamin A intoxication or administration of retinoids for dermatologic conditions. Previous studies of the mechanism of action of retinoids in non-chondrogenic cells ...
Known for Retinoic Acid | Chondrocyte Phenotype | Gene Expression | Messenger Rats

Key People For Muscular Dystrophy

Top KOLs in the world
#1
Eric P Hoffman
muscular dystrophy skeletal muscle gene expression
#2
Louis M Kunkel
muscular dystrophy skeletal muscle gene expression
#3
Francesco Francesco
muscular dystrophy skeletal muscle dystrophin gene
#4
Kevin P Campbell
skeletal muscle muscular dystrophy sarcoplasmic reticulum
#5
Volker W Straub
muscular dystrophy alglucosidase alfa pompe disease
#6
Jerry R Mendell
duchenne muscular dystrophy gene therapy spinal muscular atrophy

Center for Cardiovascular Research, University of Illinois at Chicago, Chicago, IL 60612, USA | Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, Illinois, USA | Department of Physiology and Biophysics, University o