Brilliant glycans and glycosylation: Seq and ye shall find

Gao, Guanwen; Li, Chen; Fan, Wenguo; Zhang, Mingtao; Li, Xinming; Chen, Wenqing; Li, Weiquan; Liang, Runzhang; Li, Zesong; Zhu, Xiao

doi:10.1016/j.ijbiomac.2021.08.054

Cited by 42 publications

(25 citation statements)

References 143 publications

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“…Studies have shown that people with schizophrenia and other psychiatric and neurological disorders have gamma oscillations in their brains ( Gao et al, 2021a , b ). But exactly how gamma oscillations are produced is not clear ( Fan et al, 2020 ; Lu W. et al, 2020 ; Song et al, 2020 ).…”

Section: Optogenetic Research Methodsmentioning

confidence: 99%

The Roles of Optogenetics and Technology in Neurobiology: A Review

Chen

Liang

et al. 2022

Front. Aging Neurosci.

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Optogenetic is a technique that combines optics and genetics to control specific neurons. This technique usually uses adenoviruses that encode photosensitive protein. The adenovirus may concentrate in a specific neural region. By shining light on the target nerve region, the photosensitive protein encoded by the adenovirus is controlled. Photosensitive proteins controlled by light can selectively allow ions inside and outside the cell membrane to pass through, resulting in inhibition or activation effects. Due to the high precision and minimally invasive, optogenetics has achieved good results in many fields, especially in the field of neuron functions and neural circuits. Significant advances have also been made in the study of many clinical diseases. This review focuses on the research of optogenetics in the field of neurobiology. These include how to use optogenetics to control nerve cells, study neural circuits, and treat diseases by changing the state of neurons. We hoped that this review will give a comprehensive understanding of the progress of optogenetics in the field of neurobiology.

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Section: Optogenetic Research Methodsmentioning

confidence: 99%

The Roles of Optogenetics and Technology in Neurobiology: A Review

Chen

Liang

et al. 2022

Front. Aging Neurosci.

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“…Despite undertaking enormous efforts, clinicians and drug makers are due to establish treatment options with long-lasting curative effects to patients suffering from advanced pancreatic cancer [ 35 , 36 ]. Advances in technologies in molecular and cell biology have enabled the scientific stakeholders to come up with novel targets that may overcome this long-lasting dilemma.…”

Section: Discussionmentioning

confidence: 99%

Sensory Ion Channel Candidates Inform on the Clinical Course of Pancreatic Cancer and Present Potential Targets for Repurposing of FDA-Approved Agents

Shi

Wartmann

et al. 2022

JPM

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Background: Transient receptor potential channels (TRPs) have been demonstrated to take on functions in pancreatic adenocarcinoma (PAAD) biology. However, little data are available that validate the potential of TRP in a clinical translational setting. Methods: A TRPs-related gene signature was constructed based on the Cox regression using a TCGA-PAAD cohort and receiver operating characteristic (ROC) was used to evaluate the predictive ability of this model. Core genes of the signature were screened by a protein-to-protein interaction (PPI) network, and expression validated by two independent datasets. The mutation analysis and gene set enrichment analysis (GSEA) were conducted. Virtual interventions screening was performed to discover substance candidates for the identified target genes. Results: A four TRPs-related gene signature, which contained MCOLN1, PKD1, TRPC3, and TRPC7, was developed and the area under the curve (AUC) was 0.758. Kaplan–Meier analysis revealed that patients with elevated signature score classify as a high-risk group featuring significantly shorter recurrence free survival (RFS) time, compared to the low-risk patients (p < 0.001). The gene prediction model also had a good predictive capability for predicting shortened overall survival (OS) and disease-specific survival (DSS) (AUC = 0.680 and AUC = 0.739, respectively). GSEA enrichment revealed the core genes of the signature, TRPC3 and TRPC7, were involved in several cancer-related pathways. TRPC3 mRNA is elevated in cancer tissue compared to control tissue and augmented in tumors with lymph node invasion compared to tumors without signs of lymph node invasion. Virtual substance screening of FDA approved compounds indicates that four small molecular compounds might be potentially selective not only for TRPC3 protein but also as a potential binding partner to TRPC7 protein. Conclusions: Our computational pipeline constructed a four TRP-related gene signature that enables us to predict clinical prognostic value of hitherto unrecognized biomarkers for PAAD. Sensory ion channels TRPC3 and TRPC7 could be the potential therapeutic targets in pancreatic cancer and TRPC3 might be involved in dysregulating mitochondrial functions during PAAD genesis.

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“…In the present study, our evidence suggested that AGTR1 attenuated cellular senescence of HCC cells through activating ERK signaling, indicating AGTR1 as a drug target against HCC. HCC is still difficult to treat due to a lack of drugs targeting key dependencies ( Gao et al, 2021 ), and broad-spectrum kinase antagonists (especially sorafenib) have little benefit in HCC patients ( Kelley et al, 2021 ; Ren et al, 2021 ; Wen et al, 2021 ). Experimental evidence suggests that sorafenib enables to facilitate cellular apoptosis and senescence and mitigates angiogenesis as well as suppresses proliferation in cancer cells ( Ding et al, 2021 ; Ryoo et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Suppression of AGTR1 Induces Cellular Senescence in Hepatocellular Carcinoma Through Inactivating ERK Signaling

Wang

Cui

Gong

et al. 2022

Front. Bioeng. Biotechnol.

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Objective: Cellular senescence is an effective barrier against tumorigenesis. Hence, it is of significance to characterize key features of cellular senescence and the induction of senescence in hepatocellular carcinoma (HCC) cells via pharmacological interventions. Our study determined the biological roles as well as mechanisms of angiotensin II type I receptor (AGTR1) on cellular senescence in HCC.Methods: Lentivirus vector-mediated overexpression or knockdown of AGTR1 was conducted in HCC cells, respectively. A volume of 8 μM sorafenib was used to induce cellular senescence, and ERK was activated by 30 ng/ml ERK agonist EGF. Proliferation was evaluated via clone formation assay. HCC cell senescence was examined by flow cytometry for cell cycle, senescence-associated β-galactosidase (SA-β-gal) staining, and senescence-associated heterochromatin foci (SAHF) analysis. AGTR1, p53, p21, extracellular signal-regulated kinase (ERK), and p-ERK expression were assessed through Western blot or immunofluorescence.Results: AGTR1-knockout HCC cells displayed the attenuated proliferative capacity, G2-M phase arrest, increased expression of p53 and p21, and elevated percentages of SA-β-gal- and SAHF-positive cells. In sorafenib-exposed HCC cells, overexpressed AGTR1 enhanced the proliferative capacity and alleviated G2-M phase arrest as well as decreased p53 and p21 expression and the proportions of SA-β-gal- and SAHF-positive cells. Moreover, AGTR1 knockdown attenuated the activity of p-ERK in HCC cells, and ERK agonist ameliorated AGTR1 knockdown-induced cellular senescence.Conclusion: This study demonstrates that suppression of AGTR1 induces cellular senescence in HCC through inactivating ERK signaling. The significant synergistic effect of AGTR1 suppression and sorafenib might represent a potential combination therapy for HCC.

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Brilliant glycans and glycosylation: Seq and ye shall find

Cited by 42 publications

References 143 publications

The Roles of Optogenetics and Technology in Neurobiology: A Review

The Roles of Optogenetics and Technology in Neurobiology: A Review

Sensory Ion Channel Candidates Inform on the Clinical Course of Pancreatic Cancer and Present Potential Targets for Repurposing of FDA-Approved Agents

Suppression of AGTR1 Induces Cellular Senescence in Hepatocellular Carcinoma Through Inactivating ERK Signaling

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