scholarly journals Small Proline-Rich Protein 2A

2020 ◽  
Author(s):  
Keyword(s):  
Small Proline Rich Protein ◽  
Proline Rich Protein

scholarly journals Cardiomyocyte microRNA-150 confers cardiac protection and directly represses proapoptotic small proline–rich protein 1A

JCI Insight ◽  
2021 ◽  
Vol 6 (18) ◽  
Author(s):  
Tatsuya Aonuma ◽  
Bruno Moukette ◽  
Satoshi Kawaguchi ◽  
Nipuni P. Barupala ◽  
Marisa N. Sepúlveda ◽  
...  
Keyword(s):  
Cardiac Protection ◽  
Small Proline Rich Protein ◽  
Proline Rich Protein

scholarly journals Small proline rich protein 2a in benign and malignant liver disease

Hepatology ◽  
2014 ◽  
Vol 59 (3) ◽  
pp. 1130-1143 ◽  
Author(s):  
Yoshiaki Mizuguchi ◽  
Kumiko Isse ◽  
Susan Specht ◽  
John G. Lunz ◽  
Natasha Corbitt ◽  
...  
Keyword(s):  
Liver Disease ◽  
Malignant Liver Disease ◽  
Malignant Liver ◽  
Small Proline Rich Protein ◽  
Proline Rich Protein

Expression and Regulation of Small Proline-Rich Protein 2 in Allergic Inflammation

2005 ◽  
Vol 32 (5) ◽  
pp. 428-435 ◽  
Author(s):  
Nives Zimmermann ◽  
Matthew P. Doepker ◽  
David P. Witte ◽  
Keith F. Stringer ◽  
Patricia C. Fulkerson ◽  
...  
Keyword(s):  
Allergic Inflammation ◽  
Small Proline Rich Protein ◽  
Proline Rich Protein

Gene Detection With Carbon Nanotubes

2012 ◽  
Vol 3 (2) ◽  
Author(s):  
B. Arash ◽  
Q. Wang ◽  
N. Wu
Keyword(s):  
Carbon Nanotubes ◽  
Molecular Dynamics ◽  
Carbon Nanotube ◽  
Vibration Analysis ◽  
Practical Method ◽  
Sensitivity Index ◽  
Gene Detection ◽  
Simulation Results ◽  
Small Proline Rich Protein ◽  
Proline Rich Protein

The potential of carbon nanotubes (CNTs) as nanosensors in detection of genes through a vibration analysis is investigated with molecular dynamics. The carbon nanotube based nanosensor under investigation is wrapped by a gene whose structure includes a single strand deoxyribose nucleic acid (DNA) with a certain number of distinct nucleobases. Different genes are differentiated or detected by identifying a differentiable sensitivity index that is defined to be the shifts of the resonant frequency of the nanotube. Simulation results indicate that the nanosensor is able to differentiate distinct genes, i.e., small proline-rich protein 2 A, small proline-rich protein 2B, small proline-rich protein 2D, and small proline-rich protein 2E, with a recognizable sensitivity. The research provides a rapid, effective, and practical method for detection of genes.

scholarly journals Small proline-rich protein 1A is a gp130 pathway- and stress-inducible cardioprotective protein

2004 ◽  
Vol 23 (22) ◽  
pp. 4517-4525 ◽  
Author(s):  
Sylvain Pradervand ◽  
Hideo Yasukawa ◽  
Olivier G Muller ◽  
Harald Kjekshus ◽  
Tomoyuki Nakamura ◽  
...  
Keyword(s):  
Small Proline Rich Protein ◽  
Proline Rich Protein

Abstract 12788: Cardiac MicroRNA-150 Confers Cardioprotection by Directly Repressing Pro-apoptotic Small Proline-rich Protein 1a, Sprr1a in Cardiomyocytes

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Tatsuya Aonuma ◽  
Bruno Moukette ◽  
Nipuni P Barupala ◽  
Il-man Kim
Keyword(s):  
Mouse Model ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Left Ventricular ◽  
Cardiac Protection ◽  
Reduced Ejection Fraction ◽  
Genome Wide ◽  
Evolutionarily Conserved ◽  
Small Proline Rich Protein ◽  
Proline Rich Protein

Background and Aims: Cardiac injury induces dynamic changes in the expression of microRNAs (miRs). For example, the evolutionarily conserved miR-150 is downregulated in patients with multiple cardiovascular diseases such as myocardial infarction (MI) and cardiomyopathies, as well as in various mouse models of heart failure (HF). MiR-150 is significantly associated with HF severity and outcome in humans. Using a systemic miR-150 knockout (KO) mouse model, we previously showed that carvedilol (Carv)/β 1 -adrenergic receptor/β-arrestin1-responsive miR-150 confers cardiac protection against MI (Left side in Figure). However, the extent to which expression of miR-150 in cardiomyocytes (CMs) regulates MI is unknown and there is a lack of mechanistic insight by which CM miR-150 modulates cardiac protection. Methods and Results: Here, we demonstrate using a novel mouse model that conditional CM-specific miR-150 KO (miR-150 cKO) in mice worsens cardiac dysfunction, stress, fibrosis and apoptosis post-MI, without affecting mortality or inflammation. Genome-wide transcriptomic analysis in miR-150 cKO mouse hearts identifies small proline-rich protein 1a (sprr1a) as a novel regulatory target of miR-150. Our mouse and CM studies further reveal that sprr1a expression is upregulated in CMs isolated from ischemic myocardium and subjected to simulated ischemia/reperfusion. In contrast, its expression is downregulated in hearts and CMs by Carv. Our human heart data also show that left ventricular sprr1a is upregulated in patients with HF with reduced ejection fraction. Mechanistically, the cardioprotective roles of CM miR-150 during MI are in part attributed to the direct and functional repression of pro-apoptotic gene sprr1a in CMs (Right side in Figure). Conclusions: These findings reveal a pivotal role for the miR-150/sprr1a axis in regulating CM function post-MI, and this novel axis could be a therapeutic target for intervention in ischemic heart disease.

scholarly journals Small Proline-Rich Protein 2A and 2D Are Regulated by the RBM38-p73 Axis and Associated with p73-Dependent Suppression of Chronic Inflammation

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2829
Author(s):  
Xiangmudong Kong ◽  
Dan Wang ◽  
Wenqiang Sun ◽  
Mingyi Chen ◽  
Jinhui Chen ◽  
...  
Keyword(s):  
Chronic Inflammation ◽  
Rna Binding ◽  
Ectopic Expression ◽  
Epidermal Differentiation ◽  
Keratinocyte Differentiation ◽  
Epidermal Differentiation Complex ◽  
Weak Expression ◽  
Regulatory Loop ◽  
Small Proline Rich Protein ◽  
Proline Rich Protein

Small proline-rich protein 2A and 2D (SPRR2A and SPRR2D) provide barrier function in terminally differentiated stratified squamous epithelia through the epidermal differentiation complex. However, little is known how SPRR2A/2D expression is controlled and their role in chronic inflammation. Here, we showed that that SPRR2A/2D expression is controlled by a regulatory loop formed by RNA-binding protein RBM38 and tumor suppressor p73. Specifically, we found that SPRR2A/2D expression was induced by ectopic expression of RBM38 or p73 but suppressed by knockout of Rbm38 or p73. We also found that RBM38-mediated expression of SPRR2A/2D was p73-dependent and that induction of SPRR2A/2D during keratinocyte differentiation was dependent on both p73 and Rbm38. Additionally, we found that SPRR2A/2D expression was closely associated with p73 expression in normal and cancerous tissues. To determine the biological function of the RBM38-p73 loop potentially via SPRR2A/2D, we generated a cohort of wild-type, Rbm38−/−, Trp73+/−, and Rbm38−/−;Trp73+/− mice. We found that Rbm38−/−;Trp73+/− mice had a much shorter lifespan than that for Rbm38−/−—and to a lesser extent for Trp73+/− mice—but were less prone to spontaneous tumors than Trp73+/− or Rbm38−/− mice. We also found that Rbm38−/−;Trp73+/− mice exhibited weak expression of SPRR2A/2D in multiple tissues and were susceptible to systemic chronic inflammation, suggesting that decreased SPRR2A/2D expression is likely responsible for chronic inflammation in Rbm38−/−;Trp73+/− mice, leading to a shortened lifespan. Together, our data reveal that SPRR2A/2D are novel targets of the RBM38-p73 loop and contribute to p73-dependent suppression of chronic inflammation.

Sign in / Sign up

Export Citation Format

Share Document