Shanaka Stanislaus

2.9k total citations · 2 hit papers
20 papers, 2.3k citations indexed

About

Shanaka Stanislaus is a scholar working on Molecular Biology, Cellular and Molecular Neuroscience and Endocrinology, Diabetes and Metabolism. According to data from OpenAlex, Shanaka Stanislaus has authored 20 papers receiving a total of 2.3k indexed citations (citations by other indexed papers that have themselves been cited), including 16 papers in Molecular Biology, 5 papers in Cellular and Molecular Neuroscience and 3 papers in Endocrinology, Diabetes and Metabolism. Recurrent topics in Shanaka Stanislaus's work include Fibroblast Growth Factor Research (10 papers), Epigenetics and DNA Methylation (10 papers) and Kruppel-like factors research (9 papers). Shanaka Stanislaus is often cited by papers focused on Fibroblast Growth Factor Research (10 papers), Epigenetics and DNA Methylation (10 papers) and Kruppel-like factors research (9 papers). Shanaka Stanislaus collaborates with scholars based in United States. Shanaka Stanislaus's co-authors include Murielle M. Véniant, Jing Xu, Clarence Hale, Michelle Chen, Randy Hecht, Richard Lindberg, David J. Lloyd, Steven Vonderfecht, Todd Hager and Jinlong Chen and has published in prestigious journals such as PLoS ONE, Diabetes and The Journal of Comparative Neurology.

In The Last Decade

Shanaka Stanislaus

20 papers receiving 2.2k citations

Hit Papers

align trajectories

What are hit papers?

Hit papers significantly outperform the citation benchmark for their cohort. A paper qualifies if it has ≥500 total citations, achieves ≥1.5× the top-1% citation threshold for papers in the same subfield and year (this is the minimum needed to enter the top 1%, not the average within it), or reaches the top citation threshold in at least one of its specific research topics.

Fibroblast Growth Factor 21 Reverses Hepatic Steatosis, Increases Energy Expenditure, and Improves Insulin Sensitivity in Diet-Induced Obese Mice

2008 974 citations Jing Xu, David J. Lloyd et al. Diabetes profile →
A GIPR antagonist conjugated to GLP-1 analogues promotes weight loss with improved metabolic parameters in preclinical and phase 1 settings

2024 115 citations Murielle M. Véniant, Shu-Chen Lu et al. Nature Metabolism profile →

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name	h						Papers	Cites
Shanaka Stanislaus United States	15	1.8k	386	370	356	265	20	2.3k
Lucia Berti Germany	17	842 0.5×	514 1.3×	370 1.0×	172 0.5×	208 0.8×	31	1.6k
May Bloch-Faure France	22	1.1k 0.6×	383 1.0×	202 0.5×	542 1.5×	132 0.5×	29	2.1k
Lingguang Cui United States	15	653 0.4×	480 1.2×	170 0.5×	525 1.5×	600 2.3×	17	1.6k
Terumasa Okada United States	11	998 0.6×	483 1.3×	210 0.6×	454 1.3×	980 3.7×	14	1.7k
Christine Longuet Canada	14	772 0.4×	247 0.6×	255 0.7×	1.2k 3.3×	928 3.5×	17	1.8k
Mary Wohltmann United States	22	827 0.5×	235 0.6×	170 0.5×	146 0.4×	310 1.2×	29	1.5k
Inna Astapova United States	19	674 0.4×	245 0.6×	232 0.6×	554 1.6×	145 0.5×	34	1.4k
Cristina Alarcón United States	20	763 0.4×	216 0.6×	161 0.4×	549 1.5×	986 3.7×	31	1.5k
Marie‐France Berthault France	11	565 0.3×	363 0.9×	212 0.6×	334 0.9×	544 2.1×	12	1.2k
Stefan Amisten Sweden	26	780 0.4×	197 0.5×	86 0.2×	499 1.4×	773 2.9×	44	1.7k

Countries citing papers authored by Shanaka Stanislaus

Since Specialization

Citations

This map shows the geographic impact of Shanaka Stanislaus'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 Shanaka Stanislaus with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Shanaka Stanislaus more than expected).

Fields of papers citing papers by Shanaka Stanislaus

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Shanaka Stanislaus. 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 Shanaka Stanislaus. The network helps show where Shanaka Stanislaus may publish in the future.

Co-authorship network of co-authors of Shanaka Stanislaus

This figure shows the co-authorship network connecting the top 25 collaborators of Shanaka Stanislaus. A scholar is included among the top collaborators of Shanaka Stanislaus 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 Shanaka Stanislaus. Shanaka Stanislaus is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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20 of 20 papers shown

Véniant, Murielle M., Shu-Chen Lu, Larissa Atangan, et al.. (2024). A GIPR antagonist conjugated to GLP-1 analogues promotes weight loss with improved metabolic parameters in preclinical and phase 1 settings. Nature Metabolism. 6(2). 290–303. 115 indexed citations breakdown →

Lu, Shu-Chen, Michelle Chen, Larissa Atangan, et al.. (2021). GIPR antagonist antibodies conjugated to GLP-1 peptide are bispecific molecules that decrease weight in obese mice and monkeys. Cell Reports Medicine. 2(5). 100263–100263. 71 indexed citations

Chen, Michelle, Clarence Hale, Shanaka Stanislaus, Jing Xu, & Murielle M. Véniant. (2018). FGF21 acts as a negative regulator of bile acid synthesis. Journal of Endocrinology. 237(2). 139–152. 44 indexed citations

Stanislaus, Shanaka, Randy Hecht, Junming Yie, et al.. (2017). A Novel Fc-FGF21 With Improved Resistance to Proteolysis, Increased Affinity Toward β-Klotho, and Enhanced Efficacy in Mice and Cynomolgus Monkeys. Endocrinology. 158(5). 1314–1327. 81 indexed citations

Li, Xiaodong, Shanaka Stanislaus, Frank Asuncion, et al.. (2016). FGF21 Is Not a Major Mediator for Bone Homeostasis or Metabolic Actions of PPARα and PPARγ Agonists. Journal of Bone and Mineral Research. 32(4). 834–845. 49 indexed citations

Smith, Richard, Amy Duguay, Jennifer Weiszmann, et al.. (2013). A Novel Approach to Improve the Function of FGF21. BioDrugs. 27(2). 159–166. 19 indexed citations

Bussiere, Jeanine L., Junming Yie, E. Allen Sickmier, et al.. (2013). Polyethylene Glycol Modified FGF21 Engineered to Maximize Potency and Minimize Vacuole Formation. Bioconjugate Chemistry. 24(6). 915–925. 53 indexed citations

Véniant, Murielle M., Clarence Hale, Joan Helmering, et al.. (2012). FGF21 Promotes Metabolic Homeostasis via White Adipose and Leptin in Mice. PLoS ONE. 7(7). e40164–e40164. 124 indexed citations

Véniant, Murielle M., Renée Komorowski, Ping Chen, et al.. (2012). Long-Acting FGF21 Has Enhanced Efficacy in Diet-Induced Obese Mice and in Obese Rhesus Monkeys. Endocrinology. 153(9). 4192–4203. 124 indexed citations

10.

Hale, Clarence, Michelle Chen, Shanaka Stanislaus, et al.. (2011). Lack of Overt FGF21 Resistance in Two Mouse Models of Obesity and Insulin Resistance. Endocrinology. 153(1). 69–80. 150 indexed citations

11.

Xu, Jing, Shanaka Stanislaus, Narumol Chinookoswong, et al.. (2009). Acute glucose-lowering and insulin-sensitizing action of FGF21 in insulin-resistant mouse models—association with liver and adipose tissue effects. American Journal of Physiology-Endocrinology and Metabolism. 297(5). E1105–E1114. 289 indexed citations

12.

Miranda, Les P., Katherine A. Winters, Colin V. Gegg, et al.. (2008). Design and Synthesis of Conformationally Constrained Glucagon-Like Peptide-1 Derivatives with Increased Plasma Stability and Prolonged in Vivo Activity. Journal of Medicinal Chemistry. 51(9). 2758–2765. 71 indexed citations

13.

Xu, Jing, David J. Lloyd, Clarence Hale, et al.. (2008). Fibroblast Growth Factor 21 Reverses Hepatic Steatosis, Increases Energy Expenditure, and Improves Insulin Sensitivity in Diet-Induced Obese Mice. Diabetes. 58(1). 250–259. 974 indexed citations breakdown →

14.

Khan, Imran Mahmood, et al.. (2007). Elimination of rat spinal substance P receptor bearing neurons dissociates cardiovascular and nocifensive responses to nicotinic agonists. Neuropharmacology. 54(2). 269–279. 5 indexed citations

15.

McCormick, James A., et al.. (2006). Th-P16:329 The effect of leptin versus food restriction on lipid metabolism and atherosclerosis in ApoE-/-ApoB100/100OB-/- and LDLR-/-ApoB100/100 OB-/- mice. Atherosclerosis Supplements. 7(3). 566–566. 4 indexed citations

16.

Khan, Imran Mahmood, Hitoshi Osaka, Shanaka Stanislaus, et al.. (2003). Nicotinic acetylcholine receptor distribution in relation to spinal neurotransmission pathways. The Journal of Comparative Neurology. 467(1). 44–59. 48 indexed citations

17.

Khan, Imran Mahmood, et al.. (2002). Nicotinic receptor gene cluster on rat chromosome 8 in nociceptive and blood pressure hyperresponsiveness. Physiological Genomics. 11(2). 65–72. 7 indexed citations

18.

Khan, Imran Mahmood, Shanaka Stanislaus, Duke A. Vaughn, et al.. (2001). SPINAL NICOTINIC RECEPTOR ACTIVITY IN A GENETIC MODEL OF HYPERTENSION. Clinical and Experimental Hypertension. 23(7). 555–568. 5 indexed citations

19.

Khan, Imran Mahmood, et al.. (2001). A-85380 and Epibatidine Each Interact with Disparate Spinal Nicotinic Receptor Subtypes to Achieve Analgesia and Nociception. Journal of Pharmacology and Experimental Therapeutics. 297(1). 230–239. 39 indexed citations

20.

Minne, H, et al.. (1978). Para neoplastic parathyroid hormone secretion by the transplantable walker carcino sarcoma 256 of the rat. 215. 129. 2 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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