Early work on the ubiquitin proteasome system, an interview with Irwin Rose

Rose, Irwin A.

doi:10.1038/sj.cdd.4401700

Cited by 7 publications

(3 citation statements)

References 25 publications

(24 reference statements)

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“…It is an honour and privilege to write a short introductory editorial to lectures [1][2][3] and interviews [4][5][6] with Aaron Ciechanover, Avram Hershko and Irwin Rose, the 2004 Nobel Laureates in Chemistry, for their pioneering work on the discovery of ubiquitin-mediated protein degradation. This is an additional tribute to these scientists, in recognition of their discovery and characterisation of the ubiquitin proteasome system (UPS), made in a small laboratory by great scientists with limited material, but not intellectual, resources.…”

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confidence: 99%

Discovery of the ubiquitin proteasome system and its involvement in apoptosis

Melino¹

2005

Cell Death Differ

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confidence: 99%

Discovery of the ubiquitin proteasome system and its involvement in apoptosis

Melino¹

2005

Cell Death Differ

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“…The ubiquitin pathway regulates cell homeostasis by promoting the timely degradation of key proteins involved in regulating various vital cellular processes such as cell cycle, cell death, DNA replication and repair, transcription, and immune regulation, among numerous others [39][40][41][42][43]. Given the crucial role of the ubiquitin/26S proteasome pathway in maintaining cell homeostasis, it is not surprising that defects in the ubiquitin pathway lead to several pathological ailments such as cancer and neurodegenerative diseases, which are present leading causes of death worldwide.…”

Section: Ubiquitin and Ubiquitylationmentioning

confidence: 99%

ISG15 and ISGylation in Human Diseases

Mirzalieva

Juncker

Schwartzenburg

et al. 2022

Cells

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Type I Interferons (IFNs) induce the expression of >500 genes, which are collectively called ISGs (IFN-stimulated genes). One of the earliest ISGs induced by IFNs is ISG15 (Interferon-Stimulated Gene 15). Free ISG15 protein synthesized from the ISG15 gene is post‑translationally conjugated to cellular proteins and is also secreted by cells into the extracellular milieu. ISG15 comprises two ubiquitin-like domains (UBL1 and UBL2), each of which bears a striking similarity to ubiquitin, accounting for its earlier name ubiquitin cross-reactive protein (UCRP). Like ubiquitin, ISG15 harbors a characteristic β‑grasp fold in both UBL domains. UBL2 domain has a conserved C‑terminal Gly-Gly motif through which cellular proteins are appended via an enzymatic cascade similar to ubiquitylation called ISGylation. ISG15 protein is minimally expressed under physiological conditions. However, its IFN‑dependent expression is aberrantly elevated or compromised in various human diseases, including multiple types of cancer, neurodegenerative disorders (Ataxia Telangiectasia and Amyotrophic Lateral Sclerosis), inflammatory diseases (Mendelian Susceptibility to Mycobacterial Disease (MSMD), bacteriopathy and viropathy), and in the lumbar spinal cords of veterans exposed to Traumatic Brain Injury (TBI). ISG15 and ISGylation have both inhibitory and/or stimulatory roles in the etiology and pathogenesis of human diseases. Thus, ISG15 is considered a “double-edged sword” for human diseases in which its expression is elevated. Because of the roles of ISG15 and ISGylation in cancer cell proliferation, migration, and metastasis, conferring anti-cancer drug sensitivity to tumor cells, and its elevated expression in cancer, neurodegenerative disorders, and veterans exposed to TBI, both ISG15 and ISGylation are now considered diagnostic/prognostic biomarkers and therapeutic targets for these ailments. In the current review, we shall cover the exciting journey of ISG15, spanning three decades from the bench to the bedside.

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“…This follows our previous special issue on the 2004 Nobel Prize Lectures (copyright The Nobel Foundation 2004. http:// nobelprize.org) awarded to Aaron Ciechanover, Avram Hersko and Irwin Rose for the discovery of protein degradation. [20][21][22][23][24][25][26][27][28][29][30][31][32][33] Once again, we are indebted to The Nobel Foundation for this exceptional opportunity to provide our readers with these uniquely personal accounts. Indeed, we hope our readers will perceive the human dimension underpinning these readings and that they will stimulate enthusiasm, perseverance and determination in a new generation of researchers.…”

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confidence: 99%