D-Index & Metrics Best Publications

D-Index & Metrics D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines.

Discipline name D-index D-index (Discipline H-index) only includes papers and citation values for an examined discipline in contrast to General H-index which accounts for publications across all disciplines. Citations Publications World Ranking National Ranking
Molecular Biology D-index 56 Citations 11,863 156 World Ranking 1507 National Ranking 134

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Enzyme
  • Cancer

His primary scientific interests are in Cell biology, Molecular biology, Cyclin-dependent kinase, Cyclin-dependent kinase 2 and Cell cycle. Masatoshi Kitagawa combines subjects such as Geranylgeranyl pyrophosphate, Ubiquitin, NFKB1, Biochemistry and S phase with his study of Cell biology. His Ubiquitin ligase study in the realm of Ubiquitin connects with subjects such as Glomerulosclerosis.

His work investigates the relationship between Molecular biology and topics such as Phosphorylation that intersect with problems in Binding site and DNA damage. His Cyclin-dependent kinase research integrates issues from Cyclin E and E2F. His study in Cell cycle is interdisciplinary in nature, drawing from both Epigenetics and Kinase.

His most cited work include:

  • Long non-coding RNA ANRIL is required for the PRC2 recruitment to and silencing of p15 INK4B tumor suppressor gene (751 citations)
  • Targeted disruption of Skp2 results in accumulation of cyclin E and p27 (Kip1), polyploidy and centrosome overduplication (623 citations)
  • The consensus motif for phosphorylation by cyclin D1-Cdk4 is different from that for phosphorylation by cyclin A/E-Cdk2. (522 citations)

What are the main themes of his work throughout his whole career to date?

His primary areas of study are Cell biology, Molecular biology, Cancer research, Ubiquitin ligase and Cyclin-dependent kinase. He has researched Cell biology in several fields, including Cell cycle, Retinoblastoma protein and Biochemistry. His research investigates the connection between Molecular biology and topics such as Phosphorylation that intersect with problems in MYB.

His study looks at the relationship between Cancer research and fields such as Metastasis, as well as how they intersect with chemical problems. His Ubiquitin ligase study results in a more complete grasp of Ubiquitin. He has included themes like E2F, Kinase and Cyclin-dependent kinase 2 in his Cyclin-dependent kinase study.

He most often published in these fields:

  • Cell biology (42.86%)
  • Molecular biology (40.37%)
  • Cancer research (21.74%)

What were the highlights of his more recent work (between 2012-2021)?

  • Cell biology (42.86%)
  • Molecular biology (40.37%)
  • Cancer research (21.74%)

In recent papers he was focusing on the following fields of study:

Masatoshi Kitagawa spends much of his time researching Cell biology, Molecular biology, Cancer research, Ubiquitin ligase and Transcription factor. His studies deal with areas such as Chromatin, Retinoblastoma protein, Epigenetics and Long non-coding RNA as well as Cell biology. His Molecular biology study combines topics from a wide range of disciplines, such as Protein degradation, Cell division control protein 4, Mutant, Cyclin B and Phosphorylation.

In the subject of general Cancer research, his work in Angiogenesis is often linked to Progressive disease, thereby combining diverse domains of study. His Ubiquitin ligase study is concerned with the field of Ubiquitin as a whole. His Cyclin-dependent kinase study is focused on Cell cycle in general.

Between 2012 and 2021, his most popular works were:

  • Cell cycle regulation by long non-coding RNAs (124 citations)
  • SCF Fbxo22 -KDM4A targets methylated p53 for degradation and regulates senescence (47 citations)
  • Long Noncoding RNA ELIT-1 Acts as a Smad3 Cofactor to Facilitate TGFβ/Smad Signaling and Promote Epithelial-Mesenchymal Transition. (36 citations)

In his most recent research, the most cited papers focused on:

  • Gene
  • Enzyme
  • Cancer

His main research concerns Molecular biology, Cell biology, Transcription factor, Ubiquitin ligase and F-box protein. His biological study spans a wide range of topics, including Cell division control protein 4, Cyclin-dependent kinase 2, HEK 293 cells, Phosphorylation and Kinase. The various areas that Masatoshi Kitagawa examines in his Cell biology study include Cell cycle, Cyclin-dependent kinase inhibitor protein, Cyclin-dependent kinase and Epigenetics.

His Transcription factor research includes elements of Cell cycle checkpoint, DNA damage, Protein degradation, Small interfering RNA and Protein subunit. His Ubiquitin ligase study is concerned with Ubiquitin in general. His F-box protein research incorporates elements of Demethylase, Senescence, Cell aging, Mutant and Ectopic expression.

This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.

Best Publications

Long non-coding RNA ANRIL is required for the PRC2 recruitment to and silencing of p15(INK4B) tumor suppressor gene.

Y Kotake;T Nakagawa;K Kitagawa;S Suzuki.
Oncogene (2011)

1089 Citations

Targeted disruption of Skp2 results in accumulation of cyclin E and p27 (Kip1), polyploidy and centrosome overduplication

Keiko Nakayama;Hiroyasu Nagahama;Yohji A. Minamishima;Masaki Matsumoto.
The EMBO Journal (2000)

858 Citations

An F-box protein, FWD1, mediates ubiquitin-dependent proteolysis of β-catenin

Masatoshi Kitagawa;Shigetsugu Hatakeyama;Michiko Shirane;Masaki Matsumoto.
The EMBO Journal (1999)

713 Citations

The consensus motif for phosphorylation by cyclin D1-Cdk4 is different from that for phosphorylation by cyclin A/E-Cdk2.

M. Kitagawa;H. Higashi;H.-K. Jung;I. Suzuki-Takahashi.
The EMBO Journal (1996)

709 Citations

Evidence that reactive oxygen species do not mediate NF‐κB activation

Makio Hayakawa;Hiroshi Miyashita;Isao Sakamoto;Masatoshi Kitagawa.
The EMBO Journal (2003)

552 Citations

Skp2-mediated degradation of p27 regulates progression into mitosis.

Keiko Nakayama;Hiroyasu Nagahama;Yohji A. Minamishima;Satoshi Miyake.
Developmental Cell (2004)

393 Citations

Geranylgeranylated Rho Small GTPase(s) Are Essential for the Degradation of p27Kip1 and Facilitate the Progression from G1 to S Phase in Growth-stimulated Rat FRTL-5 Cells

Aizan Hirai;Susumu Nakamura;Yoshihiko Noguchi;Tatsuji Yasuda.
Journal of Biological Chemistry (1997)

353 Citations

Down-regulation of p27 Kip1 by Two Mechanisms, Ubiquitin-mediated Degradation and Proteolytic Processing

Michiko Shirane;Yumiko Harumiya;Noriko Ishida;Aizan Hirai.
Journal of Biological Chemistry (1999)

331 Citations

Butyrolactone I, a selective inhibitor of cdk2 and cdc2 kinase.

Kitagawa M;Okabe T;Ogino H;Matsumoto H.
Oncogene (1993)

312 Citations

Phosphorylation at serine 10, a major phosphorylation site of p27(Kip1), increases its protein stability.

Noriko Ishida;Masatoshi Kitagawa;Shigetsugu Hatakeyama;Kei-ichi Nakayama.
Journal of Biological Chemistry (2000)

286 Citations

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