Salah Abu‐Hamad

2.3k total citations
21 papers, 2.0k citations indexed

About

Salah Abu‐Hamad is a scholar working on Molecular Biology, Cellular and Molecular Neuroscience and Neurology. According to data from OpenAlex, Salah Abu‐Hamad has authored 21 papers receiving a total of 2.0k indexed citations (citations by other indexed papers that have themselves been cited), including 16 papers in Molecular Biology, 5 papers in Cellular and Molecular Neuroscience and 4 papers in Neurology. Recurrent topics in Salah Abu‐Hamad's work include Mitochondrial Function and Pathology (11 papers), ATP Synthase and ATPases Research (8 papers) and Cell death mechanisms and regulation (6 papers). Salah Abu‐Hamad is often cited by papers focused on Mitochondrial Function and Pathology (11 papers), ATP Synthase and ATPases Research (8 papers) and Cell death mechanisms and regulation (6 papers). Salah Abu‐Hamad collaborates with scholars based in Israel, United States and United Kingdom. Salah Abu‐Hamad's co-authors include Varda Shoshan‐Barmatz, Adrian Israelson, Hilal Zaid, Edna Nahon, Sara Sivan, Ilana Nathan, Nurit Keinan, Lior Aram, Nir Arbel and Doron Calo and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Journal of Biological Chemistry and Neuron.

In The Last Decade

Salah Abu‐Hamad

21 papers receiving 2.0k citations

Peers

Countries citing papers authored by Salah Abu‐Hamad

Since Specialization

Citations

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

Fields of papers citing papers by Salah Abu‐Hamad

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Salah Abu‐Hamad. 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 Salah Abu‐Hamad. The network helps show where Salah Abu‐Hamad may publish in the future.

Co-authorship network of co-authors of Salah Abu‐Hamad

This figure shows the co-authorship network connecting the top 25 collaborators of Salah Abu‐Hamad. A scholar is included among the top collaborators of Salah Abu‐Hamad 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 Salah Abu‐Hamad. Salah Abu‐Hamad 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

#	Work	Indexed citations
1	Targeting the Mitochondrial Protein VDAC1 as a Potential Therapeutic Strategy in ALS 2022 ·International Journal of Molecular Sciences ·Anna Shteinfer‐Kuzmine, (unknown), (unknown), Uttpal Anand, Salah Abu‐Hamad, Ran Zalk, Varda Shoshan‐Barmatz, Adrian Israelson	23
2	A VDAC1-Derived N-Terminal Peptide Inhibits Mutant SOD1-VDAC1 Interactions and Toxicity in the SOD1 Model of ALS 2019 ·Frontiers in Cellular Neuroscience ·Anna Shteinfer‐Kuzmine, (unknown), (unknown), (unknown), Salah Abu‐Hamad, (unknown), (unknown), Andrea Magrì, Angela Messina, Elena N. Kozlova, Varda Shoshan‐Barmatz, Adrian Israelson	33
3	MIF inhibits the formation and toxicity of misfolded SOD1 amyloid aggregates: implications for familial ALS 2018 ·Cell Death and Disease ·(unknown), Victor Banerjee, (unknown), Tom Shani, Joy Kahn, Salah Abu‐Hamad, Niv Papo, Stanislav Engel, Jürgen Bernhagen, Adrian Israelson	55
4	Misfolded SOD1 Accumulation and Mitochondrial Association Contribute to the Selective Vulnerability of Motor Neurons in Familial ALS: Correlation to Human Disease 2017 ·ACS Chemical Neuroscience ·Salah Abu‐Hamad, Joy Kahn, (unknown), Jonathan D. Rosenblatt, Adrian Israelson	22
5	Macrophage Migration Inhibitory Factor as a Chaperone Inhibiting Accumulation of Misfolded SOD1 2015 ·Neuron ·Adrian Israelson, Dara Ditsworth, Shuying Sun, SungWon Song, Jason Liang, Marián Hruška-Plocháň, Melissa McAlonis‐Downes, Salah Abu‐Hamad, (unknown), Tom Shani, (unknown), Anh Thu Bui, Michael Navarro, Huilin Zhou, Martin Maršala, Brian K. Kaspar, Sandrine Da Cruz, Don W. Cleveland	99
6	Macrophage migration inhibitory factor as a component of selective vulnerability of motor neurons in ALS 2015 ·PubMed ·Salah Abu‐Hamad, Adrian Israelson	3
7	Apoptosis is regulated by the VDAC1 N-terminal region and by VDAC oligomerization: release of cytochrome c, AIF and Smac/Diablo 2010 ·Biochimica et Biophysica Acta (BBA) - Bioenergetics ·Varda Shoshan‐Barmatz, Nurit Keinan, Salah Abu‐Hamad, (unknown), Lior Aram	124
8	Dominant-negative VDAC1 mutants reveal oligomeric VDAC1 to be the active unit in mitochondria-mediated apoptosis 2010 ·Biochemical Journal ·(unknown), Salah Abu‐Hamad, Nir Arbel, (unknown), Varda Shoshan‐Barmatz	11
9	The VDAC1 N-terminus is essential both for apoptosis and the protective effect of anti-apoptotic proteins 2009 ·Journal of Cell Science ·Salah Abu‐Hamad, Nir Arbel, Doron Calo, (unknown), Adrian Israelson, Nurit Keinan, Ronit Ben-Romano, (unknown), Varda Shoshan‐Barmatz	196
10	Key regions of VDAC1 functioning in apoptosis induction and regulation by hexokinase 2008 ·Biochimica et Biophysica Acta (BBA) - Bioenergetics ·Varda Shoshan‐Barmatz, (unknown), (unknown), Salah Abu‐Hamad	108
11	Hexokinase-I Protection against Apoptotic Cell Death Is Mediated via Interaction with the Voltage-dependent Anion Channel-1 2008 ·Journal of Biological Chemistry ·Salah Abu‐Hamad, Hilal Zaid, Adrian Israelson, Edna Nahon, Varda Shoshan‐Barmatz	229
12	Mapping the ruthenium red-binding site of the voltage-dependent anion channel-1 2007 ·Cell Calcium ·Adrian Israelson, Hilal Zaid, Salah Abu‐Hamad, Edna Nahon, Varda Shoshan‐Barmatz	43
13	An N‐terminal nucleotide‐binding site in VDAC1: Involvement in regulating mitochondrial function 2007 ·Journal of Cellular Physiology ·Galit Yehezkel, Salah Abu‐Hamad, Varda Shoshan‐Barmatz	25
14	Localization of the voltage-dependent anion channel-1 Ca2+-binding sites 2006 ·Cell Calcium ·Adrian Israelson, Salah Abu‐Hamad, Hilal Zaid, Edna Nahon, Varda Shoshan‐Barmatz	64
15	The expression level of the voltage-dependent anion channel controls life and death of the cell 2006 ·Proceedings of the National Academy of Sciences ·Salah Abu‐Hamad, Sara Sivan, Varda Shoshan‐Barmatz	208
16	The voltage-dependent anion channel-1 modulates apoptotic cell death 2005 ·Cell Death and Differentiation ·Hilal Zaid, Salah Abu‐Hamad, Adrian Israelson, Ilana Nathan, Varda Shoshan‐Barmatz	258
17	A Photoactivable Probe for Calcium Binding Proteins 2005 ·Chemistry & Biology ·Adrian Israelson, (unknown), Salah Abu‐Hamad, Vladimir Khodorkovsky, Varda Shoshan‐Barmatz	23
18	Fluoxetine (Prozac) interaction with the mitochondrial voltage‐dependent anion channel and protection against apoptotic cell death 2005 ·FEBS Letters ·Edna Nahon, Adrian Israelson, Salah Abu‐Hamad, Varda Shoshan‐Barmatz	81
19	In self-defence: hexokinase promotes voltage-dependent anion channel closure and prevents mitochondria-mediated apoptotic cell death 2004 ·Biochemical Journal ·(unknown), Adrian Israelson, Salah Abu‐Hamad, Varda Shoshan‐Barmatz	332
20	In self-defense: Hexokinase promotes VDAC closure and prevents mitochondria-mediated apoptotic cell death 2003 ·Adrian Israelson, Salah Abu‐Hamad, Varda Shoshan‐Barmatz	10

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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