Helena Ostolaza

5.1k total citations · 1 hit paper
56 papers, 3.5k citations indexed

About

Helena Ostolaza is a scholar working on Molecular Biology, Surgery and Genetics. According to data from OpenAlex, Helena Ostolaza has authored 56 papers receiving a total of 3.5k indexed citations (citations by other indexed papers that have themselves been cited), including 40 papers in Molecular Biology, 18 papers in Surgery and 15 papers in Genetics. Recurrent topics in Helena Ostolaza's work include Lipid Membrane Structure and Behavior (22 papers), Lipoproteins and Cardiovascular Health (17 papers) and Escherichia coli research studies (14 papers). Helena Ostolaza is often cited by papers focused on Lipid Membrane Structure and Behavior (22 papers), Lipoproteins and Cardiovascular Health (17 papers) and Escherichia coli research studies (14 papers). Helena Ostolaza collaborates with scholars based in Spain, United States and France. Helena Ostolaza's co-authors include César Martı́n, Kepa B. Uribe, Asier Benito‐Vicente, Unai Galicia-García, Shifa Jebari, Asier Larrea‐Sebal, Félix M. Goñi, Aitziber L. Cortajarena, Fernando de la Cruz and Laura Bakás and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Journal of Biological Chemistry and PLoS ONE.

In The Last Decade

Helena Ostolaza

56 papers receiving 3.5k 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.

Pathophysiology of Type 2 Diabetes Mellitus

2020 1.9k citations Unai Galicia-García, Asier Benito‐Vicente et al. International Journal of Molecular Sciences profile →

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
Helena Ostolaza Spain	28	1.3k	872	722	520	441	56	3.5k
César Martı́n Spain	31	1.7k 1.2×	1.2k 1.4×	1.3k 1.8×	693 1.3×	592 1.3×	129	5.2k
Nicholas Murgolo United States	30	1.8k 1.3×	340 0.4×	1.5k 2.1×	329 0.6×	299 0.7×	64	4.3k
Ravinder K. Gill United States	38	2.2k 1.6×	211 0.2×	1.3k 1.8×	627 1.2×	457 1.0×	142	4.6k
Kepa B. Uribe Spain	17	793 0.6×	869 1.0×	655 0.9×	451 0.9×	206 0.5×	42	2.6k
Robert C. Cooksey United States	47	2.7k 2.0×	573 0.7×	1.1k 1.6×	1.3k 2.5×	268 0.6×	109	7.3k
Edward T. Morgan United States	46	2.3k 1.7×	894 1.0×	369 0.5×	679 1.3×	455 1.0×	120	7.7k
Noboru Okamura Japan	32	1.0k 0.8×	139 0.2×	410 0.6×	138 0.3×	160 0.4×	142	3.8k
Michael B. Fessler United States	46	2.1k 1.6×	232 0.3×	980 1.4×	954 1.8×	190 0.4×	133	5.9k
Yoshinori Fujimura Japan	36	1.5k 1.1×	221 0.3×	406 0.6×	303 0.6×	177 0.4×	157	4.1k
Mary J. Kennett United States	29	1.6k 1.2×	163 0.2×	161 0.2×	475 0.9×	352 0.8×	72	3.9k

Countries citing papers authored by Helena Ostolaza

Since Specialization

Citations

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

Fields of papers citing papers by Helena Ostolaza

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Helena Ostolaza

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

Uribe, Kepa B., et al.. (2021). Cholesterol stimulates the lytic activity of Adenylate Cyclase Toxin on lipid membranes by promoting toxin oligomerization and formation of pores with a greater effective size. FEBS Journal. 288(23). 6795–6814. 6 indexed citations

Galicia-García, Unai, Asier Benito‐Vicente, Kepa B. Uribe, et al.. (2020). Mutation type classification and pathogenicity assignment of sixteen missense variants located in the EGF-precursor homology domain of the LDLR. Scientific Reports. 10(1). 1727–1727. 25 indexed citations

Galicia-García, Unai, Shifa Jebari, Asier Larrea‐Sebal, et al.. (2020). Statin Treatment-Induced Development of Type 2 Diabetes: From Clinical Evidence to Mechanistic Insights. International Journal of Molecular Sciences. 21(13). 4725–4725. 92 indexed citations

Martı́n, César, Kepa B. Uribe, Aitor Etxebarria, et al.. (2015). Adenylate Cyclase Toxin promotes bacterial internalisation into non phagocytic cells. Scientific Reports. 5(1). 13774–13774. 9 indexed citations

Etxebarria, Aitor, Asier Benito‐Vicente, Ana Catarina Alves, et al.. (2015). Structural analysis of APOB variants, p.(Arg3527Gln), p.(Arg1164Thr) and p.(Gln4494del), causing Familial Hypercholesterolaemia provides novel insights into variant pathogenicity. Scientific Reports. 5(1). 18184–18184. 27 indexed citations

Etxebarria, Aitor, Asier Benito‐Vicente, Ana Catarina Alves, et al.. (2014). Advantages and Versatility of Fluorescence-Based Methodology to Characterize the Functionality of LDLR and Class Mutation Assignment. PLoS ONE. 9(11). e112677–e112677. 27 indexed citations

Etxebarria, Aitor, et al.. (2014). Activity-associated effect of LDL receptor missense variants located in the cysteine-rich repeats. Atherosclerosis. 238(2). 304–312. 20 indexed citations

Uribe, Kepa B., Aitor Etxebarria, César Martı́n, & Helena Ostolaza. (2013). Calpain-Mediated Processing of Adenylate Cyclase Toxin Generates a Cytosolic Soluble Catalytically Active N-Terminal Domain. PLoS ONE. 8(6). e67648–e67648. 15 indexed citations

Uribe, Kepa B., et al.. (2013). Ca2+ Influx and Tyrosine Kinases Trigger Bordetella Adenylate Cyclase Toxin (ACT) Endocytosis. Cell Physiology and Expression of the CD11b/CD18 Integrin Major Determinants of the Entry Route. PLoS ONE. 8(9). e74248–e74248. 6 indexed citations

10.

Etxebarria, Aitor, Lourdes Palacios, Marianne Stef, et al.. (2011). Functional characterization of splicing and ligand-binding domain variants in the LDL receptor. Human Mutation. 33(1). 232–243. 35 indexed citations

11.

Sánchez‐Magraner, Lissete, Aitziber L. Cortajarena, José-Luis R. Arrondo, et al.. (2010). Interdomain Ca2+ effects in Escherichia coli α-haemolysin: Ca2+ binding to the C-terminal domain stabilizes both C- and N-terminal domains. Biochimica et Biophysica Acta (BBA) - Biomembranes. 1798(6). 1225–1233. 16 indexed citations

12.

Martı́n, César, et al.. (2009). Bordetella Adenylate Cyclase Toxin Promotes Calcium Entry into Both CD11b+ and CD11b− Cells through cAMP-dependent L-type-like Calcium Channels. Journal of Biological Chemistry. 285(1). 357–364. 19 indexed citations

13.

Sánchez‐Magraner, Lissete, Ana Rosa Viguera, José-Luis R. Arrondo, et al.. (2007). The Calcium-binding C-terminal Domain of Escherichia coli α-Hemolysin Is a Major Determinant in the Surface-active Properties of the Protein. Journal of Biological Chemistry. 282(16). 11827–11835. 51 indexed citations

14.

Sánchez‐Magraner, Lissete, Aitziber L. Cortajarena, Félix M. Goñi, & Helena Ostolaza. (2005). Membrane Insertion of Escherichia coli α-Hemolysin Is Independent from Membrane Lysis. Journal of Biological Chemistry. 281(9). 5461–5467. 31 indexed citations

15.

Cortajarena, Aitziber L., Félix M. Goñi, & Helena Ostolaza. (2002). His-859 Is an Essential Residue for the Activity and pH Dependence of Escherichia coli RTX Toxin α-Hemolysin. Journal of Biological Chemistry. 277(26). 23223–23229. 12 indexed citations

16.

Bakás, Laura, et al.. (1998). Calcium-dependent conformation of E. coli α-haemolysin. Implications for the mechanism of membrane insertion and lysis. Biochimica et Biophysica Acta (BBA) - Biomembranes. 1368(2). 225–234. 42 indexed citations

17.

Ostolaza, Helena, Laura Bakás, & Félix M. Goñi. (1997). Balance of Electrostatic and Hydrophobic Interactions in the Lysis of Model Membranes by E. coli α-Haemolysin. The Journal of Membrane Biology. 158(2). 137–145. 31 indexed citations

18.

Ostolaza, Helena, et al.. (1996). Purification of Escherichia coli Pro‐Haemolysin, and a Comparison with the Properties of Mature α‐haemolysin. European Journal of Biochemistry. 238(2). 418–422. 32 indexed citations

19.

Ostolaza, Helena, et al.. (1993). Release of lipid vesicle contents by the bacterial protein toxin α-haemolysin. Biochimica et Biophysica Acta (BBA) - Biomembranes. 1147(1). 81–88. 88 indexed citations

20.

Ostolaza, Helena, Borja Bartolomé, Juan L. Serra, Fernando de la Cruz, & Félix M. Goñi. (1991). α‐Haemolysin from E. coli purification and self‐aggregation properties. FEBS Letters. 280(2). 195–198. 50 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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