Katherine M. Sixt

806 total citations
10 papers, 593 citations indexed

About

Katherine M. Sixt is a scholar working on Molecular Biology, Cancer Research and Oncology. According to data from OpenAlex, Katherine M. Sixt has authored 10 papers receiving a total of 593 indexed citations (citations by other indexed papers that have themselves been cited), including 8 papers in Molecular Biology, 4 papers in Cancer Research and 3 papers in Oncology. Recurrent topics in Katherine M. Sixt's work include RNA modifications and cancer (4 papers), Cancer-related molecular mechanisms research (4 papers) and Peptidase Inhibition and Analysis (3 papers). Katherine M. Sixt is often cited by papers focused on RNA modifications and cancer (4 papers), Cancer-related molecular mechanisms research (4 papers) and Peptidase Inhibition and Analysis (3 papers). Katherine M. Sixt collaborates with scholars based in United States and Italy. Katherine M. Sixt's co-authors include Solomon H. Snyder, Roxanne K. Barrow, Srinivasa Subramaniam, Robert G. Mealer, Alessandro Usiello, Veenu Tripathi, Roberto Weigert, Ming Zhou, Jing Huang and Shaojian Gao and has published in prestigious journals such as Nature, Science and Proceedings of the National Academy of Sciences.

In The Last Decade

Katherine M. Sixt

10 papers receiving 588 citations

Peers

Katherine M. Sixt

MB

CMN

ONCOL

CB

NEURO

Jane Savill United Kingdom

Ana Roscic Switzerland

Shoshiro Hirayama Japan

Geng‐Xian Shi United States

John S. Bett United Kingdom

Marieke Willemse Netherlands

Raffaella Calligaris Italy

Hee-Sae Park South Korea

Elena Iavnilovitch Israel

Jane Savill United Kingdom

Katherine M. Sixt

576 ×1.2

MB

246 ×1.2

CMN

131 ×1.2

ONCOL

59 ×0.7

CB

96 ×1.2

NEURO

Citations per year, relative to Katherine M. Sixt Katherine M. Sixt (= 1×) peers Jane Savill

Countries citing papers authored by Katherine M. Sixt

Since Specialization

Citations

This map shows the geographic impact of Katherine M. Sixt's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Katherine M. Sixt with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Katherine M. Sixt more than expected).

Fields of papers citing papers by Katherine M. Sixt

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Katherine M. Sixt. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Katherine M. Sixt. The network helps show where Katherine M. Sixt may publish in the future.

Co-authorship network of co-authors of Katherine M. Sixt

This figure shows the co-authorship network connecting the top 25 collaborators of Katherine M. Sixt. A scholar is included among the top collaborators of Katherine M. Sixt based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Katherine M. Sixt. Katherine M. Sixt is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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10 of 10 papers shown

1.

Tripathi, Veenu, Katherine M. Sixt, Xuan Xu, & Ying E. Zhang. (2017). Abstract 3032: Direct regulation of alternative splicing by Smad3 through PCBP1 is essential to the tumor-promoting role of transforming growth factor beta1. Cancer Research. 77(13_Supplement). 3032–3032. 1 indexed citations

2.

Tripathi, Veenu, Katherine M. Sixt, Shaojian Gao, et al.. (2016). Direct Regulation of Alternative Splicing by SMAD3 through PCBP1 Is Essential to the Tumor-Promoting Role of TGF-β. Molecular Cell. 64(3). 549–564. 79 indexed citations

3.

Zhang, Ying, et al.. (2015). TGF‐beta Regulates Alternative Splicing of CD44 by Inducing Smad3 Binding to CD44 pre‐mRNA. The FASEB Journal. 29(S1). 1 indexed citations

4.

Sommers, Connie L., Alexandre K. Rouquette‐Jazdanian, Ana I. Robles, et al.. (2013). miRNA Signature of Mouse Helper T Cell Hyper-Proliferation. PLoS ONE. 8(6). e66709–e66709. 8 indexed citations

5.

Subramaniam, Srinivasa, Robert G. Mealer, Katherine M. Sixt, et al.. (2010). Rhes, a Physiologic Regulator of Sumoylation, Enhances Cross-sumoylation between the Basic Sumoylation Enzymes E1 and Ubc9. Journal of Biological Chemistry. 285(27). 20428–20432. 68 indexed citations

6.

Sixt, Katherine M.. (2010). A way of life. Nature. 468(7321). 1–1. 3 indexed citations

7.

Subramaniam, Srinivasa, Katherine M. Sixt, Roxanne K. Barrow, & Solomon H. Snyder. (2009). Rhes, a Striatal Specific Protein, Mediates Mutant-Huntingtin Cytotoxicity. Science. 324(5932). 1327–1330. 259 indexed citations

8.

Zhu, Shanshan, Katherine M. Sixt, Miklós Békés, et al.. (2009). Protection from Isopeptidase-Mediated Deconjugation Regulates Paralog-Selective Sumoylation of RanGAP1. Molecular Cell. 33(5). 570–580. 62 indexed citations

9.

Chakraborty, Anutosh, Michael A. Koldobskiy, Katherine M. Sixt, et al.. (2008). HSP90 regulates cell survival via inositol hexakisphosphate kinase-2. Proceedings of the National Academy of Sciences. 105(4). 1134–1139. 84 indexed citations

10.

Hu, Xiaoyi, Yongjun Dang, Karen Tenney, et al.. (2007). Regulation of c-Src Nonreceptor Tyrosine Kinase Activity by Bengamide A through Inhibition of Methionine Aminopeptidases. Chemistry & Biology. 14(7). 764–774. 28 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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