Boh-Ram Kim

419 total citations
17 papers, 345 citations indexed

About

Boh-Ram Kim is a scholar working on Molecular Biology, Oncology and Pathology and Forensic Medicine. According to data from OpenAlex, Boh-Ram Kim has authored 17 papers receiving a total of 345 indexed citations (citations by other indexed papers that have themselves been cited), including 14 papers in Molecular Biology, 7 papers in Oncology and 3 papers in Pathology and Forensic Medicine. Recurrent topics in Boh-Ram Kim's work include Cancer-related Molecular Pathways (5 papers), Cell death mechanisms and regulation (4 papers) and Angiogenesis and VEGF in Cancer (4 papers). Boh-Ram Kim is often cited by papers focused on Cancer-related Molecular Pathways (5 papers), Cell death mechanisms and regulation (4 papers) and Angiogenesis and VEGF in Cancer (4 papers). Boh-Ram Kim collaborates with scholars based in South Korea and United States. Boh-Ram Kim's co-authors include Seung Bae Rho, Sokbom Kang, Seung‐Hoon Lee, Hyun‐Jung Byun, Seung Myung Dong, Jeong Heon Lee, Sung Taek Park, Mi Sun Park, Sang‐Yoon Park and Dae-Yong Kim and has published in prestigious journals such as Biochemical and Biophysical Research Communications, Oncotarget and Gynecologic Oncology.

In The Last Decade

Boh-Ram Kim

17 papers receiving 341 citations

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
Boh-Ram Kim South Korea	13	248	79	63	36	27	17	345
Jun Su China	12	287 1.2×	113 1.4×	40 0.6×	25 0.7×	24 0.9×	21	407
Dana Yip United States	6	267 1.1×	44 0.6×	90 1.4×	45 1.3×	21 0.8×	6	456
Leiming Wang China	11	274 1.1×	120 1.5×	61 1.0×	25 0.7×	22 0.8×	14	372
Vijayabaskar Lakshmikanthan United States	8	261 1.1×	58 0.7×	54 0.9×	32 0.9×	12 0.4×	8	362
Chiara Cilibrasi United Kingdom	10	187 0.8×	75 0.9×	64 1.0×	31 0.9×	26 1.0×	15	311
C-T Yeh Taiwan	7	277 1.1×	68 0.9×	75 1.2×	28 0.8×	29 1.1×	7	389
Michael Haerter Germany	4	256 1.0×	136 1.7×	41 0.7×	45 1.3×	17 0.6×	8	471
Shuanying Yang China	10	150 0.6×	64 0.8×	79 1.3×	23 0.6×	16 0.6×	22	312
Qianhua Cao China	9	248 1.0×	128 1.6×	75 1.2×	30 0.8×	15 0.6×	14	411

Countries citing papers authored by Boh-Ram Kim

Since Specialization

Citations

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

Fields of papers citing papers by Boh-Ram Kim

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Boh-Ram Kim. 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 Boh-Ram Kim. The network helps show where Boh-Ram Kim may publish in the future.

Co-authorship network of co-authors of Boh-Ram Kim

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

All Works

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17 of 17 papers shown

Rho, Seung Bae, et al.. (2021). Novel Anti-Angiogenic and Anti-Tumour Activities of the N-Terminal Domain of NOEY2 via Binding to VEGFR-2 in Ovarian Cancer. Biomolecules & Therapeutics. 29(5). 506–518. 3 indexed citations

Lee, Ji‐Yeon, Hyunji Kim, Seung Bae Rho, et al.. (2017). TSC-22 inhibits CSF-1R function and induces apoptosis in cervical cancer. Oncotarget. 8(58). 97990–98003. 10 indexed citations

Kim, Boh-Ram, et al.. (2015). Dickkopf-3 (DKK-3) obstructs VEGFR-2/Akt/mTOR signaling cascade by interacting of β2-microglobulin (β2M) in ovarian tumorigenesis. Cellular Signalling. 27(11). 2150–2159. 14 indexed citations

Kim, Boh-Ram, Seung Myung Dong, Ji‐Hae Lee, et al.. (2014). Lysyl oxidase-like 2 (LOXL2) controls tumor-associated cell proliferation through the interaction with MARCKSL1. Cellular Signalling. 26(9). 1765–1773. 29 indexed citations

Ko, Young Bok, et al.. (2014). High-mobility group box 1 (HMGB1) protein regulates tumor-associated cell migration through the interaction with BTB domain. Cellular Signalling. 26(4). 777–783. 26 indexed citations

Park, Sung Ho, Boh-Ram Kim, Jeong Heon Lee, et al.. (2014). GABARBP down-regulates HIF-1α expression through the VEGFR-2 and PI3K/mTOR/4E-BP1 pathways. Cellular Signalling. 26(7). 1506–1513. 20 indexed citations

Ko, Young Bok, Boh-Ram Kim, Kyungsil Yoon, et al.. (2014). WIF1 can effectively co-regulate pro-apoptotic activity through the combination with DKK1. Cellular Signalling. 26(11). 2562–2572. 16 indexed citations

Park, Mi Sun, Boh-Ram Kim, Seung Myung Dong, et al.. (2014). The antihypertension drug doxazosin inhibits tumor growth and angiogenesis by decreasing VEGFR-2/Akt/mTOR signaling and VEGF and HIF-1α expression. Oncotarget. 5(13). 4935–4944. 29 indexed citations

Kim, Boh-Ram, et al.. (2014). The anti-tumor activator sMEK1 and paclitaxel additively decrease expression of HIF-1α and VEGF via mTORC1-S6K/4E-BP-dependent signaling pathways. Oncotarget. 5(15). 6540–6551. 16 indexed citations

10.

Park, Mi Sun, Boh-Ram Kim, Sokbom Kang, Dae-Yong Kim, & Seung Bae Rho. (2014). The antihypertension drug doxazosin suppresses JAK/STATs phosphorylation and enhances the effects of IFN-α/γ-induced apoptosis. Genes & Cancer. 5(11-12). 470–479. 10 indexed citations

11.

Park, Sung Taek, et al.. (2013). Tumor suppressor BLU promotes paclitaxel antitumor activity by inducing apoptosis through the down-regulation of Bcl-2 expression in tumorigenesis. Biochemical and Biophysical Research Communications. 435(1). 153–159. 13 indexed citations

12.

Rho, Seung Bae, Hyun‐Jung Byun, Boh-Ram Kim, et al.. (2013). GABAA receptor-binding protein promotes sensitivity to apoptosis induced by chemotherapeutic agents. International Journal of Oncology. 42(5). 1807–1814. 8 indexed citations

13.

Park, Sung Taek, Boh-Ram Kim, Sung Ho Park, et al.. (2013). Suppression of VEGF expression through interruption of the HIF-1α and Akt signaling cascade modulates the anti-angiogenic activity of DAPK in ovarian carcinoma cells. Oncology Reports. 31(2). 1021–1029. 18 indexed citations

14.

Kim, Boh-Ram, Hye‐Jin Shin, Jooyoung Kim, et al.. (2012). Dickkopf-1 (DKK-1) interrupts FAK/PI3K/mTOR pathway by interaction of carbonic anhydrase IX (CA9) in tumorigenesis. Cellular Signalling. 24(7). 1406–1413. 15 indexed citations

15.

Byun, Hyun‐Jung, et al.. (2012). sMEK1 enhances gemcitabine anti-cancer activity through inhibition of phosphorylation of Akt/mTOR. APOPTOSIS. 17(10). 1095–1103. 20 indexed citations

16.

Park, Sung Ho, Jeong Heon Lee, Hyun‐Jung Byun, et al.. (2011). PDCD6 additively cooperates with anti-cancer drugs through activation of NF-κB pathways. Cellular Signalling. 24(3). 726–733. 24 indexed citations

17.

Rho, Seung Bae, Boh-Ram Kim, & Sokbom Kang. (2010). A gene signature-based approach identifies thioridazine as an inhibitor of phosphatidylinositol-3′-kinase (PI3K)/AKT pathway in ovarian cancer cells. Gynecologic Oncology. 120(1). 121–127. 74 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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