Solly Weiler

8.8k total citations · 5 hit papers
37 papers, 6.9k citations indexed

About

Solly Weiler is a scholar working on Molecular Biology, Physiology and Oncology. According to data from OpenAlex, Solly Weiler has authored 37 papers receiving a total of 6.9k indexed citations (citations by other indexed papers that have themselves been cited), including 28 papers in Molecular Biology, 9 papers in Physiology and 7 papers in Oncology. Recurrent topics in Solly Weiler's work include Lysosomal Storage Disorders Research (8 papers), Glycosylation and Glycoproteins Research (6 papers) and Cell death mechanisms and regulation (6 papers). Solly Weiler is often cited by papers focused on Lysosomal Storage Disorders Research (8 papers), Glycosylation and Glycoproteins Research (6 papers) and Cell death mechanisms and regulation (6 papers). Solly Weiler collaborates with scholars based in United States, Canada and Italy. Solly Weiler's co-authors include Stanley J. Korsmeyer, Michael C. Wei, Tullia Lindsten, Mona Ashiya, Kyoung Joon Oh, Michael C. Bassik, Loren D. Walensky, Anthony Letai, Emily H. Cheng and Richard A. Flavell and has published in prestigious journals such as Science, Proceedings of the National Academy of Sciences and Journal of Biological Chemistry.

In The Last Decade

Solly Weiler

34 papers receiving 6.8k citations

Hit Papers

5 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.

BCL-2, BCL-XL Sequester BH3 Domain-Only Molecules Preventing BAX- and BAK-Mediated Mitochondrial Apoptosis

2001 1.4k citations Emily H. Cheng, Michael C. Wei et al. Molecular Cell profile →
Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics

2002 1.3k citations Anthony Letai, Michael C. Bassik et al. Cancer Cell profile →
tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c

2000 1.0k citations Michael C. Wei, Tullia Lindsten et al. profile →
A Distinct Pathway Remodels Mitochondrial Cristae and Mobilizes Cytochrome c during Apoptosis

2002 890 citations Luca Scorrano, Mona Ashiya et al. Developmental Cell profile →
Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c

2000 827 citations S J Korsmeyer, Michael C. Wei et al. Cell Death and Differentiation profile →

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
Solly Weiler United States	18	5.6k	971	941	805	747	37	6.9k
Ronald Jemmerson United States	28	5.6k 1.0×	839 0.9×	1.0k 1.1×	832 1.0×	589 0.8×	71	7.4k
Sylvie Montessuit Switzerland	27	5.9k 1.0×	691 0.7×	865 0.9×	791 1.0×	599 0.8×	38	7.0k
Douglas K. Miller United States	15	4.1k 0.7×	904 0.9×	1.5k 1.6×	471 0.6×	512 0.7×	17	5.8k
Greg M. Brothers Canada	12	6.3k 1.1×	1.0k 1.1×	880 0.9×	567 0.7×	732 1.0×	13	7.5k
Grant Dewson Australia	46	5.3k 0.9×	1.1k 1.1×	1.3k 1.4×	999 1.2×	537 0.7×	81	7.2k
Hubert Hug Germany	28	4.8k 0.9×	1.3k 1.4×	1.5k 1.6×	505 0.6×	590 0.8×	42	6.7k
John P. Vaillancourt Canada	19	6.4k 1.1×	1.2k 1.3×	1.6k 1.7×	844 1.0×	941 1.3×	24	8.3k
Henning R. Stennicke Denmark	29	6.6k 1.2×	1.5k 1.5×	1.5k 1.6×	933 1.2×	909 1.2×	56	8.9k
Atan Gross Israel	25	7.0k 1.2×	1.4k 1.5×	1.5k 1.5×	1.2k 1.4×	646 0.9×	32	8.8k
Deepak Nijhawan United States	19	6.8k 1.2×	1.4k 1.5×	1.2k 1.3×	981 1.2×	749 1.0×	28	9.1k

Countries citing papers authored by Solly Weiler

Since Specialization

Citations

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

Fields of papers citing papers by Solly Weiler

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Solly Weiler

This figure shows the co-authorship network connecting the top 25 collaborators of Solly Weiler. A scholar is included among the top collaborators of Solly Weiler 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 Solly Weiler. Solly Weiler 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

Ding, Jian, Ekta Patel, Rashmi Choudhary, et al.. (2018). Abstract 3589: Preclinical evaluation of mesothelin-specific T cell receptor (TCR) fusion constructs (TRuC™s) utilizing the signaling power of the complete TCR complex: A new opportunity for solid tumor therapy. Cancer Research. 78(13_Supplement). 3589–3589. 2 indexed citations

Proia, Theresa A., Feng Jiang, Richard Nicoletti, et al.. (2015). 23814, an Inhibitory Antibody of Ligand-Mediated Notch1 Activation, Modulates Angiogenesis and Inhibits Tumor Growth without Gastrointestinal Toxicity. Molecular Cancer Therapeutics. 14(8). 1858–1867. 8 indexed citations

Meetze, Kristan, Sylvie Vincent, Steve Bottega, et al.. (2014). Neuregulin 1 Expression Is a Predictive Biomarker for Response to AV-203, an ERBB3 Inhibitory Antibody, in Human Tumor Models. Clinical Cancer Research. 21(5). 1106–1114. 41 indexed citations

Bai, Ailin, Kristan Meetze, William M. Winston, et al.. (2010). GP369, an FGFR2-IIIb–Specific Antibody, Exhibits Potent Antitumor Activity against Human Cancers Driven by Activated FGFR2 Signaling. Cancer Research. 70(19). 7630–7639. 123 indexed citations

Huérou, Yvan Le, Indrani W. Gunawardana, Allen A. Thomas, et al.. (2007). Prodrug thiamine analogs as inhibitors of the enzyme transketolase. Bioorganic & Medicinal Chemistry Letters. 18(2). 505–508. 20 indexed citations

Letai, Anthony, et al.. (2002). Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics. Cancer Cell. 2(3). 183–192. 1298 indexed citations breakdown →

Scorrano, Luca, Mona Ashiya, Karolyn Buttle, et al.. (2002). A Distinct Pathway Remodels Mitochondrial Cristae and Mobilizes Cytochrome c during Apoptosis. Developmental Cell. 2(1). 55–67. 890 indexed citations breakdown →

Cheng, Emily H., Michael C. Wei, Solly Weiler, et al.. (2001). BCL-2, BCL-XL Sequester BH3 Domain-Only Molecules Preventing BAX- and BAK-Mediated Mitochondrial Apoptosis. Molecular Cell. 8(3). 705–711. 1386 indexed citations breakdown →

Weiler, Solly, Carla Cuniberti, Kyoung Tai No, et al.. (2001). Backbone Dynamics for the Wild Type and a Double H52R/T56W Mutant of the vnd/NK-2 Homeodomain from Drosophila melanogaster. Biochemistry. 40(40). 12004–12012. 7 indexed citations

10.

Korsmeyer, S J, Michael C. Wei, Mitsuyoshi Saito, et al.. (2000). Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c. Cell Death and Differentiation. 7(12). 1166–1173. 827 indexed citations breakdown →

11.

Weiler, Solly, et al.. (1998). Site-directed Mutations in the vnd/NK-2 Homeodomain. Journal of Biological Chemistry. 273(18). 10994–11000. 38 indexed citations

12.

Xiang, Bosong, Solly Weiler, Marshall W. Nirenberg, & James A. Ferretti. (1998). Structural basis of an embryonically lethal single Ala → Thr mutation in the vnd/NK-2 homeodomain. Proceedings of the National Academy of Sciences. 95(13). 7412–7416. 12 indexed citations

13.

Weiler, Solly, et al.. (1995). Identification of the binding and activating sites of the sphingolipid activator protein, saposin C, with glucocerebrosidase. Protein Science. 4(4). 756–764. 26 indexed citations

14.

Barranger, J. A., et al.. (1995). Molecular biology of glucocerebrosidase and the treatment of Gaucher disease.. PubMed. 1(3). 149–63. 1 indexed citations

15.

Kinoshita, Haruyuki, et al.. (1995). Position of the sulfhydryl group and the disulfide bonds of human glucocerebrosidase. Journal of Protein Chemistry. 14(3). 127–137. 2 indexed citations

16.

Weiler, Solly, et al.. (1994). Assignment of a Human Melanoma Associated Gene MG50 (D2S448) to Chromosome 2p25.3 by Fluorescence in Situ Hybridization. Genomics. 22(1). 243–244. 11 indexed citations

17.

Weiler, Solly, David B. Teplow, Yasuo Kishimoto, et al.. (1993). Synthesis and characterization of a bioactive 82-residue sphingolipid activator protein, saposin C. Journal of Molecular Neuroscience. 4(3). 161–172. 9 indexed citations

18.

Ohashi, Toya, et al.. (1990). Sequence of Two Alleles Responsible for Gaucher Disease. DNA and Cell Biology. 9(4). 233–241. 74 indexed citations

19.

Morimoto, Satoshi, Yasuo Kishimoto, Solly Weiler, et al.. (1990). Saposins (Sphingolipid Activator Proteins) in the Twitcher Mutant Mouse. Journal of Neurochemistry. 55(5). 1659–1662. 1 indexed citations

20.

Weiler, Solly, et al.. (1988). The preparation of poly (dT)-5'-transferrin conjugates and hybridisation studies with poly (dA)-tailed linearised pBR322 plasmid DNA. Biochemical Pharmacology. 37(12). 2405–2410. 1 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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