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Slc2a6 regulates myoblast differentiation by targeting LDHB
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This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Type 2 diabetes mellitus often leads to muscle atrophy driven by diminished differentiation capacity in myoblasts. Myogenesis is complex, and while many involved pathways have been described, there may still be yet undiscovered therapeutic targets. With this goal in mind, a recent study combined experiments in diabetic mice and cultured myoblasts to identify key proteins in diabetes-induced atrophy. The gene for the relatively undescribed solute carrier Slc2a6, also known as glut6, was up-regulated during myogenic differentiation and down-regulated during diabetes-induced myopathy. Silencing Slc2a6 with RNAi in cell culture impaired differentiation and myotube formation. Transcriptomics and metabolomics revealed that Slc2a6 silencing disproportionally impacted the glycolysis pathway . Further experiments and analysis determined that Slc2a6 regulates myogenic differentiation in cultured myoblasts and that this regulation was partly through the glycolysis pathway..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Subject:
Biology
Life Science
Material Type:
Diagram/Illustration
Reading
Provider:
Research Square
Provider Set:
Video Bytes
Date Added:
04/14/2023
The enzyme HK2 is a potential regulator of osteoarthritis
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CC BY
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This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Patients with osteoarthritis typically experience progressive cartilage degeneration, joint inflammation, and bony growth around the joints. Treatment of this painful condition remains difficult because the underlying mechanisms aren’t clear, but recent evidence suggests that an increase in aerobic glycolysis, a form of glucose metabolism, may play a role. Aerobic glycolysis is regulated in part by the enzyme hexokinase 2 (HK2), which is upregulated in the joint tissues of patients with osteoarthritis . In addition to participating in glycolysis, HK2 affects cell growth, proliferation, survival, organelle recycling, and death under the influences of various other osteoarthritis-related proteins and pathways. For example, HK2 activity is promoted by the PI3K/Akt pathway, which is activated in osteoarthritis cartilage and HK2 might activate the transcription factor NF-κB to encourage downstream inflammatory processes in joints..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Subject:
Biology
Life Science
Material Type:
Diagram/Illustration
Reading
Provider:
Research Square
Provider Set:
Video Bytes
Date Added:
04/14/2023
miRNAs in follicular fluid exosomes regulate follicular dysplasia in PCOS
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CC BY
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This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Polycystic ovary syndrome (PCOS) is a common endocrine disease usually accompanied by infertility. In PCOS, granulosa cells (GCs) produce insufficient energy via glycolysis to support proper follicle (egg-releasing sac) development, resulting in a condition called follicular dysplasia. miRNAs in small vesicles (exosomes) within the follicular fluid can regulate GCs, but whether these miRNAs affect GC glycolysis in PCOS is unclear. To find out, a recent study sequenced the RNA in exosomes from clinical follicular fluid samples. Compared to controls, exosomes from patients with PCOS had higher levels of the miRNA miR-143-3p and lower levels of the miRNA miR-155-5p. Glycolysis pathways were also negatively regulated in PCOS exosomes. In vitro, experiments on a KGN cell PCOS model confirmed that miR-143-3p inhibited glycolysis by silencing the gene HK2. miR-155-5p normally blocks miR-143-3p’s activity, so the miR-155-5p downregulation in PCOS permitted miR-143-3p to silence HK2..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Subject:
Biology
Life Science
Material Type:
Diagram/Illustration
Reading
Provider:
Research Square
Provider Set:
Video Bytes
Date Added:
05/18/2022