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Institution

Johns Hopkins University School of Medicine

HealthcareBaltimore, Maryland, United States
About: Johns Hopkins University School of Medicine is a healthcare organization based out in Baltimore, Maryland, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 44277 authors who have published 79222 publications receiving 4788882 citations.


Papers
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Journal ArticleDOI
TL;DR: Serum prostate specific antigen levels do not reflect tumor burden and pathological stage accurately in individual patients for 2 reasons: 1) the unpredictable contribution from the benign prostatic hyperplasia component of the gland and 2) the decreasing production of prostatespecific antigen by higher grade lesions as tumor volume increases.

590 citations

Journal ArticleDOI
TL;DR: It is shown that Bace1 regulates the process of myelination and myelin sheath thickness in the central and peripheral nerves and that processed neuregulin-1 regulates myelinations by means of phosphorylation of Akt in myelin-forming cells.
Abstract: Bace1 is an endopeptidase that cleaves the amyloid precursor protein at the beta-secretase site. Apart from this cleavage, the functional importance of Bace1 in other physiological events is unknown. We show here that Bace1 regulates the process of myelination and myelin sheath thickness in the central and peripheral nerves. In Bace1-null mice, the process of myelination was delayed and myelin thickness was markedly reduced, indicating that genetic deletion of Bace1 causes hypomyelination. Bace1-null mice also showed altered neurological behaviors such as elevated pain sensitivity and reduced grip strength. Further mechanistic studies showed an altered neuregulin-Akt signaling pathway in Bace1-null mice. Full-length neuregulin-1 was increased and its cleavage product was decreased in the CNS of Bace1-null mice. Furthermore, phosphorylated Akt was also reduced. Based upon these and previous studies, we postulate that neuronally enriched Bace1 cleaves neuregulin-1 and that processed neuregulin-1 regulates myelination by means of phosphorylation of Akt in myelin-forming cells.

590 citations

Journal ArticleDOI
TL;DR: These studies demonstrated: (i) CHIP28 water channel activity is retained despite substitution of individual cysteines with serine; (ii) cysteine 189 is the Hg(2+)-sensitive residue; (iii) the subunits of theCHIP28 complex are individually active water pores; and (iv) residue 189 is critical to proper processing of the CHip28 protein.

590 citations

Journal ArticleDOI
TL;DR: The human connexin 43 gene, or GJA1, is located at human chromosome 6q22-q23 within the candidate region for the oculodentodigital dysplasia locus as mentioned in this paper.
Abstract: Gap junctions are assemblies of intercellular channels that regulate a variety of physiologic and developmental processes through the exchange of small ions and signaling molecules. These channels consist of connexin family proteins that allow for diversity of channel composition and conductance properties. The human connexin 43 gene, or GJA1, is located at human chromosome 6q22-q23 within the candidate region for the oculodentodigital dysplasia locus. This autosomal dominant syndrome presents with craniofacial (ocular, nasal, and dental) and limb dysmorphisms, spastic paraplegia, and neurodegeneration. Syndactyly type III and conductive deafness can occur in some cases, and cardiac abnormalities are observed in rare instances. We found mutations in the GJA1 gene in all 17 families with oculodentodigital dysplasia that we screened. Sixteen different missense mutations and one codon duplication were detected. These mutations may cause misassembly of channels or alter channel conduction properties. Expression patterns and phenotypic features of gja1 animal mutants, reported elsewhere, are compatible with the pleiotropic clinical presentation of oculodentodigital dysplasia.

589 citations

Journal ArticleDOI
TL;DR: The activation profile described represents a neuropathological alteration in a sizeable fraction of cases with autism, and microglial activation may play a central role in the pathogenesis of autism in a substantial proportion of patients.

589 citations


Authors

Showing all 44754 results

NameH-indexPapersCitations
Robert Langer2812324326306
Bert Vogelstein247757332094
Solomon H. Snyder2321222200444
Steven A. Rosenberg2181204199262
Kenneth W. Kinzler215640243944
Hagop M. Kantarjian2043708210208
Mark P. Mattson200980138033
Stuart H. Orkin186715112182
Paul G. Richardson1831533155912
Aaron R. Folsom1811118134044
Gonçalo R. Abecasis179595230323
Jie Zhang1784857221720
Daniel R. Weinberger177879128450
David Baker1731226109377
Eliezer Masliah170982127818
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023149
2022622
20216,078
20205,107
20194,444
20183,848