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Journal Photo for Nature
Peer reviewed only Open Access

Nature (Nature)

Publisher : Springer Nature
Multidisciplinary
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e-ISSN 1476-4687
p-ISSN 0028-0836
Issue Frequency weekly
Est. Year 1924
Mobile 02078334000
DOI YES
Language English
APC YES
Impact Factor Assignee Google Scholar
Email nature@nature.com

Journal Descriptions

Nature is a weekly international journal publishing the finest peer-reviewed research in all fields of science and technology on the basis of its originality, importance, interdisciplinary interest, timeliness, accessibility, elegance and surprising conclusions. Nature also provides rapid, authoritative, insightful and arresting news and interpretation of topical and coming trends affecting science, scientists and the wider public.

Nature (Nature) is :-

  • International, Peer-Reviewed, Open Access, Refereed, Multidisciplinary , Online or Print , weekly Journal

  • UGC Approved, ISSN Approved: P-ISSN P-ISSN: 0028-0836, E-ISSN: 1476-4687, Established: 1924,
  • Provides Crossref DOI

  • Not indexed in Scopus, WoS, DOAJ, PubMed, UGC CARE

Indexing

Publications of Nature

Somatic deletion and duplication of genes on chromosome 11 in Wilms' tumours
Bert Vogelstein May, 1984
One of the most provocative findings in tumour biology is the relationship between chromosomal changes and embryonal cancers in children. For example, children with the rare paediatric syndr...
A deadly inheritance
Bert Vogelstein December, 1990
THE p53 gene has led a short experimental life, but one filled with intrigue and irony. The latest twist is reported in two papers, one in Science1 and one that appears on page 747 of this i...
A spatial model predicts that dispersal and cell turnover limit intratumour heterogeneity
Bert Vogelstein August, 2015
Most cancers in humans are large, measuring centimetres in diameter, and composed of many billions of cells1. An equivalent mass of normal cells would be highly heterogeneous as a result of ...
CpG methylation is maintained in human cancer cells lacking DNMT1
Bert Vogelstein April, 2000
Hypermethylation is associated with the silencing of tumour susceptibility genes in several forms of cancer1,2; however, the mechanisms responsible for this aberrant methylation are poorly u...
Heteroplasmic mitochondrial DNA mutations in normal and tumour cells
Bert Vogelstein March, 2010
The presence of hundreds of copies of mitochondrial DNA (mtDNA) in each human cell poses a challenge for the complete characterization of mtDNA genomes by conventional sequencing technologie...
Inactivation of hCDC4 can cause chromosomal instability
Bert Vogelstein March, 2004
Aneuploidy, an abnormal chromosome number, has been recognized as a hallmark of human cancer for nearly a century1; however, the mechanisms responsible for this abnormality have remained elu...
Mutations in a signalling pathway
Bert Vogelstein August, 2005
Protein kinases are enzymes that are important for controlling cellular growth and invasion1, and their malfunction is implicated in the development of some tumours. We analysed human colore...
Clonal expansion of p53 mutant cells is associated with brain tumour progression
Bert Vogelstein February, 1992
TUMOUR progression is a fundamental feature of the biology of cancer1. Cancers do not arise de novo in their final form, but begin as small, indolent growths, which gradually acquire charact...
Uncoupling of S phase and mitosis induced by anticancer agents in cells lacking p21
Bert Vogelstein June, 1996
PRECISE coordination of the S and M phases of the eukaryotic cell cycle is critical not only for normal cell division, but also for effective growth arrest under conditions of stress. When d...
14-3-3σ is required to prevent mitotic catastrophe after DNA damage
Bert Vogelstein October, 1999
14-3-3σ is a member of a family of proteins that regulate cellular activity by binding and sequestering phosphorylated proteins. It has been suggested that 14-3-3σ promotes pre-mitotic cel...