About: Thomas Braun

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An Entity of Type : wikibase:Item, within Data Space : wikidata.demo.openlinksw.com associated with source document(s)

researcher (ORCID 0000-0002-6165-4804)

Attributes	Values
rdf:type	Item
description	forskare (sv) 연구원 (ko) গবেষক (bn) 研究者 (ja) ഗവേഷകൻ (ml) araştırmacı (tr) वैज्ञानिक (hi) изилдөөчү (ky) 研究者 (zh) հետազոտող (hy) hulumtues (sq) onderzoeker (nl) researcher (ORCID 0000-0002-6165-4804) (en)
rdfs:label	توماس براون (ar) Thomas Braun (en) Thomas Braun (es) Thomas Braun (nl) Thomas Braun (sl) Thomas Braun (ast)
skos:prefLabel	توماس براون (ar) Thomas Braun (en) Thomas Braun (es) Thomas Braun (nl) Thomas Braun (sl) Thomas Braun (ast)
name	توماس براون (ar) Thomas Braun (en) Thomas Braun (es) Thomas Braun (nl) Thomas Braun (sl) Thomas Braun (ast)
Scopus author ID	wds:Q40760364-C30EA4EC-55EC-4C28-9583-54A59D18BF55
AE member ID	wds:Q40760364-4BE4DF4E-385B-4988-85F8-C022CDB8870E
Scopus author ID	35432839500
AE member ID	Braun_Thomas
given name	wds:Q40760364-567CF483-975F-4322-B55E-5B51410C1C22
given name	Thomas
instance of	wds:Q40760364-99DD6A67-FF97-46C9-AEFC-4542D5B1AD3D
instance of	Homo sapiens
Hamburger Professo...essorenkatalog ID	wds:Q40760364-EBDE0A7D-EA28-4E37-B185-CC2FA75B61E8
Hamburger Professo...essorenkatalog ID	00003436
occupation	wds:Q40760364-38913DAA-C712-46DE-9AE6-FE3288BD10C2
employer	wds:Q40760364-9EA93ACE-EF21-44B3-9931-522F051CF9C1
sex or gender	wds:Q40760364-75A3280B-C199-4E3F-9FAB-844020A31001
member of	wds:Q40760364-9629EEFC-E38C-4B80-8667-1A02FB04441C
date of birth	wds:Q40760364-45F3F250-8ACA-450C-9940-E854E91736FE
family name	wds:Q40760364-D232A8EA-0C8F-4035-BC6D-56A18E947E69
occupation	researcher
employer	Max Planck Institute for Heart and Lung Research
sex or gender	male
member of	Academia Europaea
date of birth	1961-01-01 00:00:00Z (xsd:dateTime)
family name	Braun
ORCID iD	wds:Q40760364-411A4950-4CD0-4531-8BF2-7BA042E71F73
ORCID iD	https://orcid.org/0000-0002-6165-4804
ORCID iD	0000-0002-6165-4804
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q40760364
is author of	Directed expression of dominant-negative p73 enables proliferation of cardiomyocytes in mice Differential expression of myogenic determination genes in muscle cells: possible autoactivation by the Myf gene products Transcriptional mechanisms regulating skeletal muscle differentiation, growth and homeostasis. miR-1/133a clusters cooperatively specify the cardiomyogenic lineage by adjustment of myocardin levels during embryonic heart development The myogenic factor Myf5 supports efficient skeletal muscle regeneration by enabling transient myoblast amplification Epigenetic modifications of stem cells: a paradigm for the control of cardiac progenitor cells. Myf-6, a new member of the human gene family of myogenic determination factors: evidence for a gene cluster on chromosome 12 A novel human muscle factor related to but distinct from MyoD1 induces myogenic conversion in 10T1/2 fibroblasts Atheroprotective communication between endothelial cells and smooth muscle cells through miRNAs High mobility group protein-mediated transcription requires DNA damage marker γ-H2AX. Global protein expression profiling of zebrafish organs based on in vivo incorporation of stable isotopes. The sirtuin SIRT6 regulates stress granule formation in C. elegans and mammals A role for FGF-6 in skeletal muscle regeneration. The homeobox gene Lbx1 specifies a subpopulation of cardiac neural crest necessary for normal heart development NSCL-1 and NSCL-2 synergistically determine the fate of GnRH-1 neurons and control necdin gene expression Optimized, highly efficient transfer of foreign genes into newborn mouse hearts in vivo. Divergent siblings: E2F2 and E2F4 but not E2F1 and E2F3 induce DNA synthesis in cardiomyocytes without activation of apoptosis. Cellular cardiomyoplasty: improvement of left ventricular function correlates with the release of cardioactive cytokines Genetic analysis of interactions between the somitic muscle, cartilage and tendon cell lineages during mouse development Development and pathology of pulmonary hypertension. Myf5-positive satellite cells contribute to Pax7-dependent long-term maintenance of adult muscle stem cells. Evidence for a signal peptide at the amino-terminal end of human mitochondrial aldehyde dehydrogenase Uncommitted precursor cells might contribute to increased incidence of embryonal rhabdomyosarcoma in heterozygous Patched1-mutant mice Inactivation of Myf-6 and Myf-5 genes in mice leads to alterations in skeletal muscle development Myostatin mutation associated with gross muscle hypertrophy in a child Regulation of cardiomyocyte polyploidy and multinucleation by CyclinG1. Obesity-induced overexpression of miRNA-143 inhibits insulin-stimulated AKT activation and impairs glucose metabolism Acquisition of the contractile phenotype by murine arterial smooth muscle cells depends on the Mir143/145 gene cluster A new level of complexity: the role of microRNAs in cardiovascular development. Identification of right heart-enriched genes in a murine model of chronic outflow tract obstruction VITO-1, a novel vestigial related protein is predominantly expressed in the skeletal muscle lineage. VITO-2, a new SID domain protein, is expressed in the myogenic lineage during early mouse embryonic development. VITO-1, a novel vestigial related protein is predominantly expressed in the skeletal muscle lineage Cardiomyocyte-specific IκB kinase (IKK)/NF-κB activation induces reversible inflammatory cardiomyopathy and heart failure. Neurofibromin (Nf1) is required for skeletal muscle development Inactivation of MyoD in mice leads to up-regulation of the myogenic HLH gene Myf-5 and results in apparently normal muscle development. The neuronal basic helix-loop-helix transcription factor NSCL-1 is dispensable for normal neuronal development. NSCL-1 and -2 control the formation of precerebellar nuclei by orchestrating the migration of neuronal precursor cells. Targeted inactivation of the muscle regulatory gene Myf-5 results in abnormal rib development and perinatal death Inhibition of muscle differentiation by the adenovirus E1a protein: repression of the transcriptional activating function of the HLH protein Myf-5 Partial induction of the myogenic program in noncommitted adult stem cells. Therapeutic targeting of the oncostatin M receptor-β prevents inflammatory heart failure

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