Lorraine A. Everett

5.1k total citations · 1 hit paper
23 papers, 3.7k citations indexed

About

Lorraine A. Everett is a scholar working on Sensory Systems, Molecular Biology and Otorhinolaryngology. According to data from OpenAlex, Lorraine A. Everett has authored 23 papers receiving a total of 3.7k indexed citations (citations by other indexed papers that have themselves been cited), including 13 papers in Sensory Systems, 10 papers in Molecular Biology and 6 papers in Otorhinolaryngology. Recurrent topics in Lorraine A. Everett's work include Hearing, Cochlea, Tinnitus, Genetics (13 papers), Ion Transport and Channel Regulation (8 papers) and Ear Surgery and Otitis Media (6 papers). Lorraine A. Everett is often cited by papers focused on Hearing, Cochlea, Tinnitus, Genetics (13 papers), Ion Transport and Channel Regulation (8 papers) and Ear Surgery and Otitis Media (6 papers). Lorraine A. Everett collaborates with scholars based in United States, United Kingdom and Netherlands. Lorraine A. Everett's co-authors include Eric D. Green, Inès Royaux, Susan M. Wall, Eric D. Green, Koichi Suzuki, Val C. Sheffield, Faiad Adawi, John C. Beck, Jacquelyn R. Idol and Benjamin Gläser and has published in prestigious journals such as Cell, Proceedings of the National Academy of Sciences and Nature Genetics.

In The Last Decade

Lorraine A. Everett

23 papers receiving 3.6k 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.

Pendred syndrome is caused by mutations in a putative sulphate transporter gene (PDS)

1997 866 citations Lorraine A. Everett, Benjamin Gläser et al. Nature Genetics profile →

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
Lorraine A. Everett United States	19	1.9k	1.7k	963	610	541	23	3.7k
Inès Royaux United States	22	1.4k 0.8×	686 0.4×	437 0.5×	180 0.3×	405 0.7×	27	2.6k
Daryl A. Scott United States	32	1.9k 1.0×	842 0.5×	464 0.5×	316 0.5×	174 0.3×	97	3.9k
Raquel Rabionet Spain	27	2.1k 1.1×	1.5k 0.9×	520 0.5×	201 0.3×	56 0.1×	65	3.4k
Hideichi Shinkawa Japan	27	609 0.3×	1.2k 0.7×	757 0.8×	516 0.8×	22 0.0×	105	2.1k
Xiaorui Shi China	30	755 0.4×	1.6k 1.0×	1.1k 1.2×	183 0.3×	16 0.0×	104	2.8k
Julio Contreras Spain	20	878 0.5×	459 0.3×	215 0.2×	44 0.1×	180 0.3×	47	2.1k
Lily Ng United States	30	2.1k 1.1×	451 0.3×	264 0.3×	26 0.0×	1.4k 2.5×	56	3.8k
Kimia Kahrizi Iran	30	1.8k 1.0×	826 0.5×	382 0.4×	174 0.3×	51 0.1×	141	3.0k
Jacqueline E. Lee United States	17	1.8k 1.0×	256 0.2×	231 0.2×	26 0.0×	364 0.7×	18	3.0k
Leonardo D’Agruma Italy	18	833 0.4×	671 0.4×	205 0.2×	86 0.1×	48 0.1×	46	1.8k

Countries citing papers authored by Lorraine A. Everett

Since Specialization

Citations

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

Fields of papers citing papers by Lorraine A. Everett

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Lorraine A. Everett. 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 Lorraine A. Everett. The network helps show where Lorraine A. Everett may publish in the future.

Co-authorship network of co-authors of Lorraine A. Everett

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

1.

Kim, Young Hee, Vladimír Pech, William H. Beierwaltes, et al.. (2007). Reduced ENaC protein abundance contributes to the lower blood pressure observed in pendrin-null mice. American Journal of Physiology-Renal Physiology. 293(4). F1314–F1324. 88 indexed citations

2.

Jabba, Sairam V., Ruchira Singh, Rajanikanth J Maganti, et al.. (2006). Macrophage invasion contributes to degeneration of stria vascularis in Pendred syndrome mouse model. BMC Medicine. 4(1). 37–37. 56 indexed citations

3.

Verlander, Jill W., Young Hee Kim, Truyen D. Pham, et al.. (2006). Dietary Cl⁻restriction upregulates pendrin expression within the apical plasma membrane of type B intercalated cells. American Journal of Physiology-Renal Physiology. 291(4). F833–F839. 77 indexed citations

4.

Pech, Vladimír, Young Hee Kim, Alan M. Weinstein, et al.. (2006). Angiotensin II increases chloride absorption in the cortical collecting duct in mice through a pendrin-dependent mechanism. American Journal of Physiology-Renal Physiology. 292(3). F914–F920. 98 indexed citations

5.

Kim, Young‐Hee, Jill W. Verlander, Sharon W. Matthews, et al.. (2005). Intercalated cell H⁺/OH⁻transporter expression is reduced inSlc26a4null mice. American Journal of Physiology-Renal Physiology. 289(6). F1262–F1272. 37 indexed citations

6.

Wangemann, Philine, Tao Wu, Sairam V. Jabba, et al.. (2004). Loss of KCNJ10 protein expression abolishes endocochlear potential and causes deafness in Pendred syndrome mouse model. BMC Nephrology. 2(30). 1 indexed citations

7.

Wangemann, Philine, Tao Wu, Sairam V. Jabba, et al.. (2004). Loss of KCNJ10 protein expression abolishes endocochlear potential and causes deafness in Pendred syndrome mouse model. BMC Medicine. 2(1). 30–30. 211 indexed citations

8.

Royaux, Inès, Inna A. Belyantseva, Tao Wu, et al.. (2003). Localization and Functional Studies of Pendrin in the Mouse Inner Ear Provide Insight About the Etiology of Deafness in Pendred Syndrome. Journal of the Association for Research in Otolaryngology. 4(3). 394–404. 124 indexed citations

9.

Suzuki, Koichi, Inès Royaux, Lorraine A. Everett, et al.. (2002). Expression ofPDS/Pds, the Pendred Syndrome Gene, in Endometrium. The Journal of Clinical Endocrinology & Metabolism. 87(2). 938–938. 49 indexed citations

10.

Karniski, Lawrence P., Tong Wang, Lorraine A. Everett, et al.. (2002). Formate-stimulated NaCl absorption in the proximal tubule is independent of the pendrin protein. American Journal of Physiology-Renal Physiology. 283(5). F952–F956. 12 indexed citations

11.

Royaux, Inès, Susan M. Wall, Lawrence P. Karniski, et al.. (2001). Pendrin, encoded by the Pendred syndrome gene, resides in the apical region of renal intercalated cells and mediates bicarbonate secretion. Proceedings of the National Academy of Sciences. 98(7). 4221–4226. 436 indexed citations

12.

Everett, Lorraine A., et al.. (2000). The <i>PDS</i> Gene, Pendred Syndrome and Non-Syndromic Deafness (DFNB4). Advances in oto-rhino-laryngology. 56. 145–151. 9 indexed citations

13.

Royaux, Inès, Koichi Suzuki, Atsumi Mori, et al.. (2000). Pendrin, the Protein Encoded by the Pendred Syndrome Gene (PDS), Is an Apical Porter of Iodide in the Thyroid and Is Regulated by Thyroglobulin in FRTL-5 Cells. Endocrinology. 141(2). 839–845. 315 indexed citations

14.

Coucke, Paul, Peter Van Hauwe, Lorraine A. Everett, et al.. (1999). Identification of two different mutations in the PDS gene in an inbred family with Pendred syndrome. Journal of Medical Genetics. 36(6). 475–477. 40 indexed citations

15.

Everett, Lorraine A., et al.. (1999). Expression pattern of the mouse ortholog of the Pendred’s syndrome gene ( Pds ) suggests a key role for pendrin in the inner ear. Proceedings of the National Academy of Sciences. 96(17). 9727–9732. 236 indexed citations

16.

Cremers, C. W. R. J., R.J.C. Admiraal, Lorraine A. Everett, et al.. (1998). Progressive Sensorineural Hearing Loss and a Widened Vestibular Aqueduct in Pendred Syndrome. Archives of Otolaryngology - Head and Neck Surgery. 124(5). 501–501. 59 indexed citations

17.

Cremers, Cor W. R. J., R.J.C. Admiraal, P.L.M. Huygen, et al.. (1998). Progressive hearing loss, hypoplasia of the cochlea and widened vestibular aqueducts are very common features in Pendred’s syndrome. International Journal of Pediatric Otorhinolaryngology. 45(2). 113–123. 74 indexed citations

18.

Hauwe, Peter Van, Lorraine A. Everett, Paul Coucke, et al.. (1998). Two Frequent Missense Mutations in Pendred Syndrome. Human Molecular Genetics. 7(7). 1099–1104. 143 indexed citations

19.

Everett, Lorraine A., Benjamin Gläser, John C. Beck, et al.. (1997). Pendred syndrome is caused by mutations in a putative sulphate transporter gene (PDS). Nature Genetics. 17(4). 411–422. 866 indexed citations breakdown →

20.

Morris, Colleen A., Carolyn Β. Mervis, Jacquelyn Bertrand, et al.. (1996). LIM-kinase1 Hemizygosity Implicated in Impaired Visuospatial Constructive Cognition. Cell. 86(1). 59–69. 411 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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