Characterization of somatostatin receptors and associated signaling pathways in pancreas of R6/2 transgenic mice

: Central dogma of molecular biology has remained cornerstone of classical molecular biology but serendipitous discovery of microRNAs (miRNAs) in nematodes paradigmatically shifted our current understanding of the intricate mech-anisms which occur during transitions from transcription to translation. Discovery of miRNA captured tremendous attention and appreciation and we had witnessed an explosion in the field of non-coding RNAs. Ground-breaking discoveries in the field of non-coding RNAs have helped in better characterization of microRNAs and long non-coding RNAs (LncRNAs). There is an ever-increasing list of miRNA targets which are regulated by MALAT1 to stimulate or repress expression of tar-get genes. However, in this review our main focus is to summarize mechanistic insights related to MALAT1-mediated regu-lation of oncogenic signaling pathways. We have discussed how MALAT1 modulated TGF/SMAD and Hippo pathways in various cancers. We have also comprehensively summarized how JAK/STAT and Wnt/β-catenin pathways stimulated MALAT1 expression and consequentially how MALAT1 potentiated these signaling cascades to promote cancer. MALAT1 research has undergone substantial broadening however, there is still a need to identify additional mechanisms. MALAT1 is involved in multi-layered regulation of multiple transduction cascades and detailed analysis of different pathways will be helpful in getting a step closer to individualized medicine.

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Characterization of starvation-induced autophagy in cerebellar Purkinje cells of pHluorin-mKate2-human LC3B transgenic mice

Scientific Reports ◽

10.1038/s41598-020-66370-6 ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Juan Alejandro Oliva Trejo ◽

Isei Tanida ◽

Chigure Suzuki ◽

Soichiro Kakuta ◽

Norihiro Tada ◽

...

Keyword(s):

Transgenic Mice ◽

Purkinje Cells ◽

Cerebellar Purkinje Cells

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Molecular Pathogenesis of Hodgkin Lymphoma: Past, Present, Future

International Journal of Molecular Sciences ◽

10.3390/ijms21186623 ◽

2020 ◽

Vol 21 (18) ◽

pp. 6623 ◽

Cited By ~ 1

Author(s):

Marc Bienz ◽

Salima Ramdani ◽

Hans Knecht

Keyword(s):

Immune System ◽

Targeted Therapy ◽

Signaling Pathways ◽

Hodgkin Lymphoma ◽

Genetic Instability ◽

Host Immune System ◽

Cellular Interactions ◽

Classical Hodgkin Lymphoma ◽

The Past

Our understanding of the tumorigenesis of classical Hodgkin lymphoma (cHL) and the formation of Reed–Sternberg cells (RS-cells) has evolved drastically in the last decades. More recently, a better characterization of the signaling pathways and the cellular interactions at play have paved the way for new targeted therapy in the hopes of improving outcomes. However, important gaps in knowledge remain that may hold the key for significant changes of paradigm in this lymphoma. Here, we discuss the past, present, and future of cHL, and review in detail the more recent discoveries pertaining to genetic instability, anti-apoptotic signaling pathways, the tumoral microenvironment, and host-immune system evasion in cHL.

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Transcriptomic and Metabolic Network Analysis of Metabolic Reprogramming and IGF-1 Modulation in SCA3 Transgenic Mice

International Journal of Molecular Sciences ◽

10.3390/ijms22157974 ◽

2021 ◽

Vol 22 (15) ◽

pp. 7974

Author(s):

Yu-Te Lin ◽

Yong-Shiou Lin ◽

Wen-Ling Cheng ◽

Jui-Chih Chang ◽

Yi-Chun Chao ◽

...

Keyword(s):

Network Analysis ◽

Transgenic Mice ◽

Signaling Pathways ◽

Metabolic Network ◽

Metabolic Reprogramming ◽

Spinocerebellar Ataxia Type ◽

Positive Effects ◽

Metabolic Network Analysis ◽

Potential Biomarker ◽

Metabolic Remodeling

Spinocerebellar ataxia type 3 (SCA3) is a genetic neurodegenerative disease for which a cure is still needed. Growth hormone (GH) therapy has shown positive effects on the exercise behavior of mice with cerebellar atrophy, retains more Purkinje cells, and exhibits less DNA damage after GH intervention. Insulin-like growth factor 1 (IGF-1) is the downstream mediator of GH that participates in signaling and metabolic regulation for cell growth and modulation pathways, including SCA3-affected pathways. However, the underlying therapeutic mechanisms of GH or IGF-1 in SCA3 are not fully understood. In the present study, tissue-specific genome-scale metabolic network models for SCA3 transgenic mice were proposed based on RNA-seq. An integrative transcriptomic and metabolic network analysis of a SCA3 transgenic mouse model revealed that metabolic signaling pathways were activated to compensate for the metabolic remodeling caused by SCA3 genetic modifications. The effect of IGF-1 intervention on the pathology and balance of SCA3 disease was also explored. IGF-1 has been shown to invoke signaling pathways and improve mitochondrial function and glycolysis pathways to restore cellular functions. As one of the downregulated factors in SCA3 transgenic mice, IGF-1 could be a potential biomarker and therapeutic target.

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