scholarly journals Latest microscope technique for plant biology; to obtain ultrastructure, molecular mechanism, and biological function

2020 ◽  
Vol 32 (1) ◽  
pp. 1-2
Author(s):  
◽  
Kiminori Toyooka
Keyword(s):  
Molecular Mechanism ◽  
Biological Function ◽  
Plant Biology ◽  
Microscope Technique

Studying how genetic variants affect mechanism in biological systems

2018 ◽  
Vol 62 (4) ◽  
pp. 575-582
Author(s):  
Francesco Raimondi ◽  
Robert B. Russell
Keyword(s):  
Genetic Variation ◽  
Molecular Mechanism ◽  
Genetic Variants ◽  
Biological Function ◽  
Biological Systems ◽  
Protein Structures ◽  
Clinical Applications ◽  
Biological Pathways ◽  
The Relationship

Genetic variants are currently a major component of system-wide investigations into biological function or disease. Approaches to select variants (often out of thousands of candidates) that are responsible for a particular phenomenon have many clinical applications and can help illuminate differences between individuals. Selecting meaningful variants is greatly aided by integration with information about molecular mechanism, whether known from protein structures or interactions or biological pathways. In this review we discuss the nature of genetic variants, and recent studies highlighting what is currently known about the relationship between genetic variation, biomolecular function, and disease.

scholarly journals Biological function and molecular mechanism of SRSF3 in cancer and beyond (Review)

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Jian Xiong ◽  
Yinshuang Chen ◽  
Weipeng Wang ◽  
Jing Sun
Keyword(s):  
Molecular Mechanism ◽  
Biological Function

scholarly journals CircRNA1615 Inhibits Ferroptosis via Modulation of Autophagy by the miRNA152-3p/LRP6 Axis in Cardiomyocytes of Myocardial Infarction

2021 ◽  
Author(s):  
Rui-lin Li ◽  
Cheng-hui Fan ◽  
Shi-yu Gong ◽  
Sheng Kang
Keyword(s):  
Myocardial Infarction ◽  
Molecular Mechanism ◽  
Biological Function ◽  
Myocardial Cell ◽  
Pathological Process ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Gene Assay

Abstract Background Searching for new molecular targets of ferroptosis is gradually becoming the focus in the field of cardiovascular disease research. This study was aimed to explore the biological function and molecular mechanism of ferroptosis of circRNA modulation in cardiomyocytes of myocardial infarction (MI).Method We explored the regulatory effect and molecular mechanism of LPR6 on myocardial cell ferroptosis by establishing a model of MI in vivo and in vitro, constructed the regulatory network of circRNA-miRNA-LRP6 by the bioinformatics analysis, and focused on the biological function and molecular mechanism of circRNA1615 regulating ferroptosis in MI by the overexpression or knockdown of circRNA1615, the RIP experiments, and double luciferase reporter gene assay.Results Ferrostatin-1(ferroptosis inhibitor) can improve the pathological process of MI; LRP6 was involved in the process of ferroptosis in cardiomyocytes; LRP6 deletion regulates ferroptosis in cardiomyocytes through autophagy; Screening and identification of circRNA1615 targets LRP6; circRNA1615 inhibits ferroptosis in cardiomyocytes; circRNA1615 regulates the expression of LRP6 through sponge adsorption of miR-152-3p, and then prevent LRP6-mediated autophagy-related ferroptosis in cardiomyocytes, finally regulate the pathological process of MI.Conclusions CircRNA1615 inhibits ferroptosis via modulation of autophagy by the miRNA152-3p/LRP6 molecular axis in cardiomyocytes of myocardial infarction.

scholarly journals Gpn2 and Rba50 Directly Participate in the Assembly of the Rpb3 Sub-complex in the Biogenesis of RNA Polymerase II

2018 ◽  
pp. MCB.00091-18 ◽  
Author(s):  
Fanli Zeng ◽  
Yu Hua ◽  
Xiaoqin Liu ◽  
Sijie Liu ◽  
Kejing Lao ◽  
...  
Keyword(s):  
Cell Growth ◽  
Rna Polymerase ◽  
Rna Polymerase Ii ◽  
Organizational Development ◽  
Molecular Mechanism ◽  
Biological Function ◽  
Macromolecular Complex ◽  
Clear Definition ◽  
Two Factors ◽  
Definition Of

RNA polymerase II (RNAPII) is one of the central enzymes in cell growth and organizational development. It is a large macromolecular complex consisting of twelve subunits. Relative to the clear definition of RNAPII structure and biological function, the molecular mechanism of how RNAPII is assembled is poorly understood, because of that the key assembly factors acting for the assembly of RNAPII remain elusive. In this study, we identified two factors, Gpn2 and Rba50, which directly participate in the assembly of RNAPII. Gpn2 and Rba50 were demonstrated to interact with Rpb12 and Rpb3, respectively. The interaction between Gpn2 and Rba50 was also demonstrated. When Gpn2 and Rba50 are functionally defective, the assembly of the Rpb3 sub-complex is disrupted, leading to defect in the assembly of RNAPII. Based on these results, we conclude that Gpn2 and Rba50 directly participate in the assembly of the Rpb3 sub-complex and subsequently the biogenesis of RNAPII.

scholarly journals Circ-SOX4 drives the tumorigenesis and development of lung adenocarcinoma via sponging miR-1270 and modulating PLAGL2 to activate WNT signaling pathway

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Nan Gao ◽  
Baoguo Ye
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Molecular Mechanism ◽  
Biological Function ◽  
Wnt Signaling Pathway ◽  
Luciferase Reporter ◽  
Invasion And Migration ◽  
And Migration

Abstract Background Lung adenocarcinoma (LUAD), a widespread histopathological subtype of lung cancer, is deemed as a malignant tumor with a peak risk of mortality. Emerged as RNA with a loop structure that depleted protein coding ability, circular RNA (circRNA) has been identified as a regulator in cancer progression. Circ-SOX4, identified as a novel circRNA, has not been studied in any cancer yet. Thus, the regulatory function that circ-SOX4 exerts on LUAD development remains obscure. Aim of the study This study aimed to investigate the biological function and molecular mechanism of circ-SOX4 in LUAD. Methods The expression of circ-SOX4 was detected by qRT-PCR. CCK-8, colony formation, transwell and wound healing assays were performed to explore the biological function of circ-SOX4 in LUAD. The interaction between miR-1270 and circ-SOX41 (or PLAGL2) was confirmed by RNA pull down, luciferase reporter and RIP assays. Results Circ-SOX4 was found to be obviously upregulated in LUAD tissues and cells, and knockdown of it inhibited cell proliferation, invasion and migration in LUAD. Furthermore, silenced circ-SOX4 also inhibited LUAD tumor growth. Molecular mechanism assays revealed that circ-SOX4 interacted with miR-1270 in LUAD. Besides, PLAGL2 was confirmed as a downstream gene of miR-1270. Rescue assays validated that miR-1270 suppression or PLAGL2 overexpression countervailed circ-SOX4 depletion-mediated inhibition on cell proliferation, invasion and migration in LUAD. Additionally, it was discovered that circ-SOX4/miR-1270/PLAGL2 axis activated WNT signaling pathway in LUAD. Conclusions Circ-SOX4 boosted the development of LUAD and activate WNT signaling pathway through sponging miR-1270 and modulating PLAGL2, which provided a valuable theoretical basis for exploring underlying therapeutic target in LUAD.

Induction of Metallothionein

1989 ◽  
Vol 8 (7) ◽  
pp. 1315-1321 ◽  
Author(s):  
Curtis D. Klaassen ◽  
Lois D. Lehman-Mckeeman
Keyword(s):  
Heavy Metals ◽  
Heavy Metal ◽  
Molecular Mechanism ◽  
Organic Compounds ◽  
Metal Binding ◽  
Binding Proteins ◽  
Biological Function ◽  
Metal Homeostasis ◽  
Pivotal Role ◽  
The Relationship

Metallothioneins (MTs) are cysteine-rich metal-binding proteins. These proteins play a pivotal role in heavy metal homeostasis and have been widely studied by biochemists, toxicologists, nutritional scientists, and molecular biologists. It is well established that MTs are inducible proteins. They are normally synthesized at low basal levels, but exposure to a wide variety of heavy metals and many organic compounds will dramatically increase synthesis of MTs. This paper summarizes MT induction by reviewing the chemicals that induce these proteins, the molecular mechanism involved in this induction, and the relationship between MT induction and biological function.

scholarly journals Fibrinogen Activates the Capture of Human Plasminogen by Staphylococcal Fibronectin-Binding Proteins

mBio ◽  
2017 ◽  
Vol 8 (5) ◽  
Author(s):  
Philippe Herman-Bausier ◽  
Giampiero Pietrocola ◽  
Timothy J. Foster ◽  
Pietro Speziale ◽  
Yves F. Dufrêne
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Surface ◽  
Molecular Mechanism ◽  
Conformational Changes ◽  
Binding Proteins ◽  
Biological Function ◽  
Surface Protein ◽  
Activation Mechanism ◽  
Human Plasminogen ◽  
Fibronectin Binding

ABSTRACT Invasive bacterial pathogens can capture host plasminogen (Plg) and allow it to form plasmin. This process is of medical importance as surface-bound plasmin promotes bacterial spread by cleaving tissue components and favors immune evasion by degrading opsonins. In Staphylococcus aureus, Plg binding is in part mediated by cell surface fibronectin-binding proteins (FnBPs), but the underlying molecular mechanism is not known. Here, we use single-cell and single-molecule techniques to demonstrate that FnBPs capture Plg by a sophisticated activation mechanism involving fibrinogen (Fg), another ligand found in the blood. We show that while FnBPs bind to Plg through weak (∼200-pN) molecular bonds, direct interaction of the adhesins with Fg through the high-affinity dock, lock, and latch mechanism dramatically increases the strength of the FnBP-Plg bond (up to ∼2,000 pN). Our results point to a new model in which the binding of Fg triggers major conformational changes in the FnBP protein, resulting in the buried Plg-binding domains being projected and exposed away from the cell surface, thereby promoting strong interactions with Plg. This study demonstrated a previously unidentified role for a ligand-binding interaction by a staphylococcal cell surface protein, i.e., changing the protein orientation to activate a cryptic biological function. IMPORTANCE Staphylococcus aureus captures human plasminogen (Plg) via cell wall fibronectin-binding proteins (FnBPs), but the underlying molecular mechanism is not known. Here we show that the forces involved in the interaction between Plg and FnBPs on the S. aureus surface are weak. However, we discovered that binding of fibrinogen to FnBPs dramatically strengthens the FnBP-Plg bond, therefore revealing an unanticipated role for Fg in the capture of Plg by S. aureus. These experiments favor a model where Fg-induced conformational changes in FnBPs promote their interaction with Plg. This work uncovers a previously undescribed activation mechanism for a staphylococcal surface protein, whereby ligand-binding elicits a cryptic biological function. IMPORTANCE Staphylococcus aureus captures human plasminogen (Plg) via cell wall fibronectin-binding proteins (FnBPs), but the underlying molecular mechanism is not known. Here we show that the forces involved in the interaction between Plg and FnBPs on the S. aureus surface are weak. However, we discovered that binding of fibrinogen to FnBPs dramatically strengthens the FnBP-Plg bond, therefore revealing an unanticipated role for Fg in the capture of Plg by S. aureus. These experiments favor a model where Fg-induced conformational changes in FnBPs promote their interaction with Plg. This work uncovers a previously undescribed activation mechanism for a staphylococcal surface protein, whereby ligand-binding elicits a cryptic biological function.

scholarly journals Biological function and molecular mechanism of piRNA in cancer

2019 ◽  
Vol 13 ◽  
pp. e00113 ◽  
Author(s):  
Ghanbar Mahmoodi Chalbatani ◽  
Hassan Dana ◽  
Feridon Memari ◽  
Elahe Gharagozlou ◽  
Shirin Ashjaei ◽  
...  
Keyword(s):  
Molecular Mechanism ◽  
Biological Function
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