Cytoplasmic domain of NCAM140 interacts with ubiquitin-fold modifier-conjugating enzyme-1 (Ufc1)

Homrich, Mirka; Wobst, Hilke; Laurini, Christine; Sabrowski, Julia; Schmitz, Brigitte; Diestel, Simone

doi:10.1016/j.yexcr.2014.04.003

Cited by 23 publications

(22 citation statements)

References 33 publications

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“…The cDNAs encoding the intracellular domain of human NCAM180 (hNCAM180-ID) and NCAM140 (hNCAM140-ID) used to produce recombinant proteins for the protein macroarray assay have been described (Homrich et al, 2014;Wobst et al, 2012).…”

Section: Dna Constructs and Sirnasmentioning

confidence: 99%

“…Expression and purification of recombinant proteins for protein macroarray hNCAM180-ID and hNCAM140-ID were expressed in BL21 (DE3) bacteria and purified by Nickel-nitrilotriacetic acid affinity chromatography (hNCAM180-ID) or by glutathione affinity chromatography (hNCAM140-ID) according to manufacturer's instructions (Qiagen) as described previously (Homrich et al, 2014;Wobst et al, 2012). Purified proteins were concentrated to a minimum of 1 mg/ml in phosphate-buffered saline (PBS) and fluorescently labeled with Dyomics DY-633 Fluorophore (Dyomics, Jena, Germany).…”

Section: Dna Constructs and Sirnasmentioning

confidence: 99%

“…The macroarray membrane (Source Bioscience imaGenes, Berlin, Germany) containing 24,000 different His-tagged expression clones of human fetal brain was prepared as described previously (Homrich et al, 2014;Wobst et al, 2012). Purified and fluorescently labeled hNCAM180-ID (15 nM) and NCAM140-ID (13.5 nM), respectively, were incubated in Odyssey blocking buffer (LI-COR Biosciences) with the prepared membrane for 16 h. Signals were detected using the Licor Odyssey scanner (LI-COR Biosciences).…”

Section: Protein Macroarraymentioning

confidence: 99%

“…Images were analyzed with Aida Image Analyzer version 4.24 (Raytest, Straubenhardt, Germany). Positive spots were identified using the Scoring Template and the annotation table of Source Bioscience imaGenes revealing the spotting pattern of the expression clones on the membrane (Homrich et al, 2014;Wobst et al, 2012).…”

Section: Protein Macroarraymentioning

confidence: 99%

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Kinesin-1 promotes post-Golgi trafficking of NCAM140 and NCAM180 to the cell surface

Wobst

Schmitz

Schachner

et al. 2015

Journal of Cell Science

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The neural cell adhesion molecule (NCAM, also known as NCAM1) is important during neural development, because it contributes to neurite outgrowth in response to its ligands at the cell surface. In the adult brain, NCAM is involved in regulating synaptic plasticity. The molecular mechanisms underlying delivery of NCAM to the neuronal cell surface remain poorly understood. We used a protein macroarray and identified the kinesin light chain 1 (KLC1), a component of the kinesin-1 motor protein, as a binding partner of the intracellular domains of the two transmembrane isoforms of NCAM, NCAM140 and NCAM180. KLC1 binds to amino acids CGKAGPGA within the intracellular domain of NCAM and colocalizes with kinesin-1 in the Golgi compartment. Delivery of NCAM180 to the cell surface is increased in CHO cells and neurons co-transfected with kinesin-1. We further demonstrate that the p21-activated kinase 1 (PAK1) competes with KLC1 for binding to the intracellular domain of NCAM and contributes to the regulation of the membrane insertion of NCAM. Our results indicate that NCAM is delivered to the cell surface through a kinesin-1-mediated transport mechanism in a PAK1-dependent manner.

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Section: Dna Constructs and Sirnasmentioning

confidence: 99%

Section: Dna Constructs and Sirnasmentioning

confidence: 99%

Section: Protein Macroarraymentioning

confidence: 99%

Section: Protein Macroarraymentioning

confidence: 99%

See 2 more Smart Citations

Kinesin-1 promotes post-Golgi trafficking of NCAM140 and NCAM180 to the cell surface

Wobst

Schmitz

Schachner

et al. 2015

Journal of Cell Science

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“…Moreover, Cdk5rap3 ufmylation seems to play a role in the regulation of the tumor suppressor activity of Cdk5rap3 17) . Intriguingly, Homrich et al observed that the overexpression of UFM1 markedly increased neural cell adhesion molecule (NCAM) endocytosis , indicating that NCAM ufmylation affects its trafficking 18) . Most recently, Yoo et al 19) demonstrated that activating signal cointegrator 1 (ASC1) is a novel target for ufmylation and ufmylation of ASC1 and plays a crucial role in the development of estrogen receptor-apositive breast cancer.…”

Section: Introductionmentioning

confidence: 99%

UFM1 Protects Macrophages from oxLDL-Induced Foam Cell Formation Through a Liver X Receptor α Dependent Pathway

Pang

Xiong

et al. 2015

JAT

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Aim: Macrophage foam cell formation is the most prominent characteristic of the early stages of atherosclerosis. Ubiquitin Fold Modifier 1 (UFM1) is a new member of the ubiquitin-like protein family, and its underlying mechanism of action in macrophage foam cell formation is poorly understood. Our current study focuses on UFM1 and investigates its role in macrophage foam cell formation. Methods: Using real-time quantitative PCR (qRT-PCR) and western blot analysis, we first analyzed the UFM1 expression in mouse peritoneal macrophages (MPMs) from ApoE / mice in vivo and in human macrophages treated with oxLDL in vitro. Subsequently, the effects of UFM1 on macrophages foam cell formation were determined by Nile Red staining and direct lipid analysis. We then examined whether UFM1 affects the process of lipid metabolism in macrophages. Lastly, with the method of small interfering RNA (siRNA), we delineated the mechanism of UFM1 to attenuate lipid accumulation in THP-1 macrophages. Results: UFM1 is dramatically upregulated under atherosclerosis conditions both in vivo and in vitro. Moreover, UFM1 markedly decreased macrophage foam cell formation. Mechanistic studies revealed that UFM1 increased the macrophage cholesterol efflux, which was due to the increased expression of ATP-binding cassette transporters A1 (ABCA1) and G1 (ABCG1). Furthermore, the upregulation of ABCA1 and ABCG1 by UFM1 resulted from liver X receptor (LXR ) activation, which was confirmed by the observation that LXR siRNA prevented the expression of ABCA1 and ABCG1. Consistent with this, the UFM1-mediated attenuation of lipid accumulation was abolished by such inhibition. Conclusions: Taken together, our results showed that UFM1 could suppress foam cell formation via the LXR -dependent pathway.

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Blood RNA transcripts reveal similar and differential alterations in fundamental cellular processes in Alzheimer's disease and other neurodegenerative diseases

Huseby

Delvaux

Brokaw

et al. 2022

Alzheimer's & Dementia

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Background Dysfunctional processes in Alzheimer's disease and other neurodegenerative diseases lead to neural degeneration in the central and peripheral nervous system. Research demonstrates that neurodegeneration of any kind is a systemic disease that may even begin outside of the region vulnerable to the disease. Neurodegenerative diseases are defined by the vulnerabilities and pathology occurring in the regions affected. Method A random forest machine learning analysis on whole blood transcriptomes from six neurodegenerative diseases generated unbiased disease‐classifying RNA transcripts subsequently subjected to pathway analysis. Results We report that transcripts of the blood transcriptome selected for each of the neurodegenerative diseases represent fundamental biological cell processes including transcription regulation, degranulation, immune response, protein synthesis, apoptosis, cytoskeletal components, ubiquitylation/proteasome, and mitochondrial complexes that are also affected in the brain and reveal common themes across six neurodegenerative diseases. Conclusion Neurodegenerative diseases share common dysfunctions in fundamental cellular processes. Identifying regional vulnerabilities will reveal unique disease mechanisms. Highlights Transcriptomics offer information about dysfunctional processes. Comparing multiple diseases will expose unique malfunctions within diseases. Blood RNA can be used ante mortem to track expression changes in neurodegenerative diseases. Protocol standardization will make public datasets compatible.

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Cytoplasmic domain of NCAM140 interacts with ubiquitin-fold modifier-conjugating enzyme-1 (Ufc1)

Cited by 23 publications

References 33 publications

Kinesin-1 promotes post-Golgi trafficking of NCAM140 and NCAM180 to the cell surface

Kinesin-1 promotes post-Golgi trafficking of NCAM140 and NCAM180 to the cell surface

UFM1 Protects Macrophages from oxLDL-Induced Foam Cell Formation Through a Liver X Receptor α Dependent Pathway

Blood RNA transcripts reveal similar and differential alterations in fundamental cellular processes in Alzheimer's disease and other neurodegenerative diseases

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