<scp>SUMO</scp>
            2 is essential while
            <scp>SUMO</scp>
            3 is dispensable for mouse embryonic development

Wang, Liangli; Wansleeben, Carolien; Zhao, Shengli; Miao, Pei; Paschen, Wulf; Yang, Wei

doi:10.15252/embr.201438534

Cited by 173 publications

(183 citation statements)

References 14 publications

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“…SUMO1 -/-mice are also viable and fertile and lack any obvious phenotype, indicating that the SUMO2 pool is able to compensate for the absence of SUMO1 [19,20]. Mating experiments between the different knockout mice further indicated that the different SUMO family members functionally compensated for each other [18]. Thus, accurate mouse development appears to require the presence of a critical level of SUMO2.…”

Section: Twenty Years Of Sumo Research In Cell Cycle Controlmentioning

confidence: 99%

“…SUMO2 is the only essential SUMO family member. SUMO2-deficient mice died early during embryonic development (embryonic day 10.5), with severe developmental defects [18]. In contrast, SUMO3 -/-mice were viable and did not show any overt defects [18].…”

Section: Twenty Years Of Sumo Research In Cell Cycle Controlmentioning

confidence: 99%

“…SUMO2-deficient mice died early during embryonic development (embryonic day 10.5), with severe developmental defects [18]. In contrast, SUMO3 -/-mice were viable and did not show any overt defects [18]. Due to their high sequence similarity in their mature forms, it is unlikely that SUMO2 and SUMO3 have major different functional properties.…”

Section: Twenty Years Of Sumo Research In Cell Cycle Controlmentioning

confidence: 99%

“…However, the two proteins show a striking difference in their expression levels. The SUMO2 mRNA accounts for 80% of the entire SUMO mRNA pool in total mouse embryos at E7.5, whereas SUMO3 is only expressed at very low levels (2%) [18]. SUMO1 -/-mice are also viable and fertile and lack any obvious phenotype, indicating that the SUMO2 pool is able to compensate for the absence of SUMO1 [19,20].…”

Section: Twenty Years Of Sumo Research In Cell Cycle Controlmentioning

confidence: 99%

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SUMOylation-Mediated Regulation of Cell Cycle Progression and Cancer

Eifler

Vertegaal

2015

Trends in Biochemical Sciences

243

211

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SUMOylation plays critical roles during cell cycle progression. Many important cell cycle regulators, including many oncogenes and tumor suppressors, are functionally regulated via SUMOylation. The dynamic SUMOylation pattern observed throughout the cell cycle is ensured via distinct spatial and temporal regulation of the SUMO machinery. Additionally, SUMOylation cooperates with other post-translational modifications to mediate cell cycle progression. Deregulation of these SUMOylation and deSUMOylation enzymes causes severe defects in cell proliferation and genome stability. Different types of cancers were recently shown to be dependent on a functioning SUMOylation system, a finding that could potentially be exploited in anti-cancer therapies. KeywordsSUMO; mitosis; SUMOylation; cancer; cell cycle SUMO: a ubiquitin-like modifier that regulates nuclear processesThe complexity of eukaryotic proteomes is widely expanded by protein processing and a vast array of posttranslational modifications. The quick and reversible attachment of small modifiers is essential for all cellular processes and ensures dynamic and rapid responses to extracellular and intracellular stimuli. Apart from chemical modifications such as phosphorylation [1], glycosylation [2] and acetylation [3], small polypeptides can be attached to proteins, resulting in a change in the activity, localization, half-life or interactome of the target protein. Since the initial discovery of ubiquitin, the founding member of these small protein posttranslational modifications in 1975 [4], a large family of structurally related ubiquitin-like modifiers has been uncovered including SUMO, Nedd8, ISG15, FAT10, FUB1, UFM1, URM1, Atg12 and Atg8 [5][6][7][8]. The attachment of these small ubiquitin-like modifiers is catalysed by an enzymatic cascade consisting of an activating enzyme (E1), a conjugating enzyme (E2) and a ligase (E3), and can be reversed by specific and cell cycle control. It is therefore not surprising that SUMO signal transduction has been implicated in the development of several different cancer types, which could potentially be exploited in anti-cancer therapies. In this review we will focus on the role of SUMO in cell cycle regulation, specifically highlighting its physiological relevance and its deregulation in cancer. Recent progress includes the identification of many novel SUMO substrates with important roles in cell cycle progression using proteomic approaches, and the demonstration that different mouse cancer models are dependent on a functioning SUMOylation system. Switching of SUMOylation in these cancer models caused a proliferation block of the cancer cells, showing that SUMO conjugating enzymes are potential drug targets. Europe PMC Funders Group Twenty years of SUMO research in cell cycle controlSUMO was linked to cell cycle progression even before the identification of the small protein modifier itself. Twenty years ago, the yeast SUMO conjugating enzyme Ubc9 was first proposed to be a ubiquitin conjugating enzyme. Ubc9 was s...

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Section: Twenty Years Of Sumo Research In Cell Cycle Controlmentioning

confidence: 99%

Section: Twenty Years Of Sumo Research In Cell Cycle Controlmentioning

confidence: 99%

Section: Twenty Years Of Sumo Research In Cell Cycle Controlmentioning

confidence: 99%

Section: Twenty Years Of Sumo Research In Cell Cycle Controlmentioning

confidence: 99%

See 2 more Smart Citations

SUMOylation-Mediated Regulation of Cell Cycle Progression and Cancer

Eifler

Vertegaal

2015

Trends in Biochemical Sciences

243

211

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“…Like in every other cell type studied so far, SUMOylation substrates are dominantly found in the nucleus of neuronal cells, but some controversy exists regarding extranuclear substrates in general and synaptic substrates in particular (Daniel et al., 2017). Nevertheless, SUMOylation has attracted increasing interest in the field of neurosciences and has been shown to regulate neuronal function under physiological and pathophysiological conditions (Krumova & Weishaupt, 2013; Wang et al., 2014; Yang & Paschen, 2015). …”

Section: Introductionmentioning

confidence: 99%

SUMO1‐conjugation is altered during normal aging but not by increased amyloid burden

et al. 2018

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SummaryA proper equilibrium of post‐translational protein modifications is essential for normal cell physiology, and alteration in these processes is key in neurodegenerative disorders such as Alzheimer's disease. Recently, for instance, alteration in protein SUMOylation has been linked to amyloid pathology. In this work, we aimed to elucidate the role of protein SUMOylation during aging and increased amyloid burden in vivo using a His6‐HA‐SUMO1 knock‐in mouse in the 5XFAD model of Alzheimer's disease. Interestingly, we did not observe any alteration in the levels of SUMO1‐conjugation related to Alzheimer's disease. SUMO1 conjugates remained localized to neuronal nuclei upon increased amyloid burden and during aging and were not detected in amyloid plaques. Surprisingly however, we observed age‐related alterations in global levels of SUMO1 conjugation and at the level of individual substrates using quantitative proteomic analysis. The identified SUMO1 candidate substrates are dominantly nuclear proteins, mainly involved in RNA processing. Our findings open novel directions of research for studying a functional link between SUMOylation and its role in guarding nuclear functions during aging.

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SUMO‐regulated transcription: Challenging the dogma

Chymkowitch

Enserink

2015

BioEssays

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The small ubiquitin-like modifier SUMO regulates many aspects of cellular physiology to maintain cell homeostasis, both under normal conditions and during cell stress. Components of the transcriptional apparatus and chromatin are among the most prominent SUMO substrates. The prevailing view is that SUMO serves to repress transcription. However, as we will discuss in this review, this model needs to be refined, because recent studies have revealed that SUMO can also have profound positive effects on transcription.

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SUMO 2 is essential while SUMO 3 is dispensable for mouse embryonic development

Cited by 173 publications

References 14 publications

SUMOylation-Mediated Regulation of Cell Cycle Progression and Cancer

SUMOylation-Mediated Regulation of Cell Cycle Progression and Cancer

SUMO1‐conjugation is altered during normal aging but not by increased amyloid burden

SUMO‐regulated transcription: Challenging the dogma

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