Maja Sochalska

480 total citations
18 papers, 360 citations indexed

About

Maja Sochalska is a scholar working on Molecular Biology, Immunology and Periodontics. According to data from OpenAlex, Maja Sochalska has authored 18 papers receiving a total of 360 indexed citations (citations by other indexed papers that have themselves been cited), including 9 papers in Molecular Biology, 8 papers in Immunology and 6 papers in Periodontics. Recurrent topics in Maja Sochalska's work include Oral microbiology and periodontitis research (6 papers), Cell death mechanisms and regulation (5 papers) and Streptococcal Infections and Treatments (4 papers). Maja Sochalska is often cited by papers focused on Oral microbiology and periodontitis research (6 papers), Cell death mechanisms and regulation (5 papers) and Streptococcal Infections and Treatments (4 papers). Maja Sochalska collaborates with scholars based in Poland, United States and Austria. Maja Sochalska's co-authors include Jan Potempa, Andreas Villunger, Susanne Kirschnek, Marco Groth, Juliane Vier, Selma Tuzlak, Alexander Egle, Eleonora Ottina, Grzegorz Bereta and Maria Chomyszyn‐Gajewska and has published in prestigious journals such as The Journal of Immunology, Oncogene and Scientific Reports.

In The Last Decade

Maja Sochalska

18 papers receiving 355 citations

Peers

Maja Sochalska

PERIO

IMMUN

PHEOH

ONCOL

Mary K. Khlgatian United States

N. Ogura Japan

Qiudong Yang China

Ellis Johnson United States

Ihachi Kato Japan

Gwennaëlle Monnot Switzerland

James E. Riggs United States

Min‐Kyoung Song South Korea

Fagui Zou China

Mariko Nakamura Japan

Mary K. Khlgatian United States

Maja Sochalska

117 ×0.8

168 ×1.4

PERIO

96 ×0.8

IMMUN

82 ×1.3

PHEOH

43 ×0.8

ONCOL

Citations per year, relative to Maja Sochalska Maja Sochalska (= 1×) peers Mary K. Khlgatian

Countries citing papers authored by Maja Sochalska

Since Specialization

Citations

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

Fields of papers citing papers by Maja Sochalska

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Maja Sochalska

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

All Works

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18 of 18 papers shown

Sochalska, Maja, et al.. (2025). Porphyromonas Gingivalis Virulence Factors and their Role in Undermining Antimicrobial Defenses and Host Cell Death Programs in the Pathobiology of Chronic Periodontal Disease. Postępy Mikrobiologii - Advancements of Microbiology. 64(1). 3–23. 1 indexed citations

Jakubowski, Witold, et al.. (2025). Porphyromonas gingivalis affects neutrophil pro-inflammatory activities. Frontiers in Cell and Developmental Biology. 13. 1419651–1419651. 1 indexed citations

Bielecka, Ewa, Karolina Marzec, Maja Sochalska, et al.. (2024). Ursolic Acid Formulations Effectively Induce Apoptosis and Limit Inflammation in the Psoriasis Models In Vitro. Biomedicines. 12(4). 732–732. 6 indexed citations

Ferdek, Paweł E., et al.. (2024). Polyethylene Glycols Stimulate Ca2+ Signaling, Cytokine Production, and the Formation of Neutrophil Extracellular Traps. International Journal of Nanomedicine. Volume 19. 13165–13181. 1 indexed citations

Potempa, Jan, et al.. (2023). Porphyromonas gingivalis Peptidyl Arginine Deiminase (PPAD) in the Context of the Feed-Forward Loop of Inflammation in Periodontitis. International Journal of Molecular Sciences. 24(16). 12922–12922. 9 indexed citations

Bzowska, Monika, et al.. (2021). Mouse IgG3 binding to macrophage-like cells is prevented by deglycosylation of the antibody or by Accutase treatment of the cells. Scientific Reports. 11(1). 10295–10295. 4 indexed citations

Potempa, Jan, et al.. (2021). Uncovering the Oral Dysbiotic Microbiota as Masters of Neutrophil Responses in the Pathobiology of Periodontitis. Frontiers in Microbiology. 12. 729717–729717. 14 indexed citations

Sochalska, Maja, et al.. (2020). Application of the In Vitro HoxB8 Model System to Characterize the Contributions of Neutrophil–LPS Interaction to Periodontal Disease. Pathogens. 9(7). 530–530. 4 indexed citations

Bereta, Grzegorz, Maja Sochalska, Katarzyna Gawron, et al.. (2019). HDAC3 Regulates Gingival Fibroblast Inflammatory Responses in Periodontitis. Journal of Dental Research. 99(1). 98–106. 27 indexed citations

10.

Bereta, Grzegorz, Maja Sochalska, Katarzyna Gawron, et al.. (2019). BET Bromodomain Inhibitors Suppress Inflammatory Activation of Gingival Fibroblasts and Epithelial Cells From Periodontitis Patients. Frontiers in Immunology. 10. 933–933. 30 indexed citations

11.

Sochalska, Maja & Jan Potempa. (2017). Manipulation of Neutrophils by Porphyromonas gingivalis in the Development of Periodontitis. Frontiers in Cellular and Infection Microbiology. 7. 197–197. 84 indexed citations

12.

Vier, Juliane, Marco Groth, Maja Sochalska, & Susanne Kirschnek. (2016). The anti-apoptotic Bcl-2 family protein A1/Bfl-1 regulates neutrophil survival and homeostasis and is controlled via PI3K and JAK/STAT signaling. Cell Death and Disease. 7(2). e2103–e2103. 66 indexed citations

13.

Sochalska, Maja, et al.. (2016). MYC selects against reduced BCL2A1/A1 protein expression during B cell lymphomagenesis. Oncogene. 36(15). 2066–2073. 17 indexed citations

14.

Ottina, Eleonora, Maja Sochalska, Roswitha Sgonc, & Andreas Villunger. (2015). The BH3-only protein Bad is dispensable for TNF-mediated cell death. Cell Death and Disease. 6(1). e1611–e1611. 3 indexed citations

15.

Sochalska, Maja, Eleonora Ottina, Selma Tuzlak, et al.. (2015). Conditional knockdown of BCL2A1 reveals rate-limiting roles in BCR-dependent B-cell survival. Cell Death and Differentiation. 23(4). 628–639. 18 indexed citations

16.

Sochalska, Maja, Selma Tuzlak, Alexander Egle, & Andreas Villunger. (2015). Lessons from gain‐ and loss‐of‐function models of pro‐survival Bcl2 family proteins: implications for targeted therapy. FEBS Journal. 282(5). 834–849. 51 indexed citations

17.

Ottina, Eleonora, Katarina Lyberg, Maja Sochalska, Andreas Villunger, & Gunnar Nilsson. (2014). Knockdown of the Antiapoptotic Bcl-2 Family Member A1/Bfl-1 Protects Mice from Anaphylaxis. The Journal of Immunology. 194(3). 1316–1322. 18 indexed citations

18.

Skjoedt, Karsten, Steen V. Petersen, Claus Koch, et al.. (2013). Three monoclonal antibodies against the serpin protease nexin-1 prevent protease translocation. Thrombosis and Haemostasis. 111(1). 29–40. 6 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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