Inbal Maniv

962 total citations
11 papers, 708 citations indexed

About

Inbal Maniv is a scholar working on Molecular Biology, Epidemiology and Genetics. According to data from OpenAlex, Inbal Maniv has authored 11 papers receiving a total of 708 indexed citations (citations by other indexed papers that have themselves been cited), including 10 papers in Molecular Biology, 3 papers in Epidemiology and 3 papers in Genetics. Recurrent topics in Inbal Maniv's work include CRISPR and Genetic Engineering (6 papers), Ubiquitin and proteasome pathways (4 papers) and Autophagy in Disease and Therapy (3 papers). Inbal Maniv is often cited by papers focused on CRISPR and Genetic Engineering (6 papers), Ubiquitin and proteasome pathways (4 papers) and Autophagy in Disease and Therapy (3 papers). Inbal Maniv collaborates with scholars based in United States, Israel and Netherlands. Inbal Maniv's co-authors include Luciano A. Marraffini, Asma Hatoum-Aslan, Wenyan Jiang, Poulami Samai, Bruce R. Levin, David Bikard, Yossi Gottfried, Sarit Larisch, María García‐Fernández and Assaf Friedler and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Journal of Biological Chemistry and Nature Communications.

In The Last Decade

Inbal Maniv

11 papers receiving 704 citations

Peers

Inbal Maniv

MB

ECOLO

GENET

EPIDE

IS

Nora C. Pyenson United States

R.E. Haurwitz United States

Robert Heler United States

Nancy Ramia United States

Beatriz A. Osuna United States

Yibei Xiao United States

Maolu Yin China

Ekaterina Savitskaya Russia

Alireza Edraki United States

Sabrina Y. Stanley Canada

Nora C. Pyenson United States

Inbal Maniv

776 ×1.2

MB

113 ×0.7

ECOLO

174 ×1.2

GENET

87 ×0.8

EPIDE

94 ×0.8

IS

Citations per year, relative to Inbal Maniv Inbal Maniv (= 1×) peers Nora C. Pyenson

Countries citing papers authored by Inbal Maniv

Since Specialization

Citations

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

Fields of papers citing papers by Inbal Maniv

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Inbal Maniv

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

All Works

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11 of 11 papers shown

1.

Maniv, Inbal, et al.. (2025). Ubiquitin C‐Terminal Hydrolase L1 (UCHL1), Beyond Hydrolysis. BioEssays. 47(8). e70028–e70028. 1 indexed citations

2.

Maniv, Inbal, Elle Koren, Noa Reis, et al.. (2023). Altered ubiquitin signaling induces Alzheimer’s disease-like hallmarks in a three-dimensional human neural cell culture model. Nature Communications. 14(1). 5922–5922. 28 indexed citations

3.

Maniv, Inbal, Wenyan Jiang, David Bikard, & Luciano A. Marraffini. (2016). Impact of Different Target Sequences on Type III CRISPR-Cas Immunity. Journal of Bacteriology. 198(6). 941–950. 40 indexed citations

4.

Veenman, L., Sukhdev Singh, Ahmad Masarwa, et al.. (2015). Quinazoline-based tricyclic compounds that regulate programmed cell death, induce neuronal differentiation, and are curative in animal models for excitotoxicity and hereditary brain disease. Cell Death Discovery. 1(1). 15027–15027. 31 indexed citations

5.

Hatoum-Aslan, Asma, Inbal Maniv, Poulami Samai, & Luciano A. Marraffini. (2013). Genetic Characterization of Antiplasmid Immunity through a Type III-A CRISPR-Cas System. Journal of Bacteriology. 196(2). 310–317. 122 indexed citations

6.

Jiang, Wenyan, et al.. (2013). Dealing with the Evolutionary Downside of CRISPR Immunity: Bacteria and Beneficial Plasmids. PLoS Genetics. 9(9). e1003844–e1003844. 163 indexed citations

7.

Maniv, Inbal, Asma Hatoum-Aslan, & Luciano A. Marraffini. (2013). CRISPR decoys. RNA Biology. 10(5). 694–699. 1 indexed citations

8.

Hatoum-Aslan, Asma, Poulami Samai, Inbal Maniv, Wenyan Jiang, & Luciano A. Marraffini. (2013). A Ruler Protein in a Complex for Antiviral Defense Determines the Length of Small Interfering CRISPR RNAs. Journal of Biological Chemistry. 288(39). 27888–27897. 95 indexed citations

9.

Gottfried, Yossi, Inbal Maniv, Marie‐Jeanne Carp, et al.. (2012). Peptides Mimicking the Unique ARTS-XIAP Binding Site Promote Apoptotic Cell Death in Cultured Cancer Cells. Clinical Cancer Research. 18(9). 2569–2578. 25 indexed citations

10.

Maniv, Inbal, et al.. (2011). The IAP-antagonist ARTS initiates caspase activation upstream of cytochrome C and SMAC/Diablo. Cell Death and Differentiation. 19(2). 356–368. 46 indexed citations

11.

Hatoum-Aslan, Asma, Inbal Maniv, & Luciano A. Marraffini. (2011). Mature clustered, regularly interspaced, short palindromic repeats RNA (crRNA) length is measured by a ruler mechanism anchored at the precursor processing site. Proceedings of the National Academy of Sciences. 108(52). 21218–21222. 156 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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