Topic
PITX2
About: PITX2 is a research topic. Over the lifetime, 473 publications have been published within this topic receiving 46601 citations. The topic is also known as: ARP1 & Brx1.
Papers published on a yearly basis
Papers
TL;DR: Observations suggest that either Myf-5 or MyoD is required for the determination of skeletal myoblasts, their propagation, or both during embryonic development and indicate that these factors play, at least in part, functionally redundant roles in myogenesis.
1,824 citations
TL;DR: The results indicate that MyoD is dispensable for skeletal muscle development in mice, revealing some degree of functional redundancy in the control of the skeletal myogenic developmental program.
1,070 citations
TL;DR: The role of NF-kappaB in cytokine-induced muscle degeneration was explored and its expression was down-regulated by TNF and IFN-gamma expression in mouse muscle in vivo, elucidate a possible mechanism that may underlie the skeletal muscle decay in cachexia.
Abstract: MyoD regulates skeletal muscle differentiation (SMD) and is essential for repair of damaged tissue. The transcription factor nuclear factor kappa B (NF-kappaB) is activated by the cytokine tumor necrosis factor (TNF), a mediator of skeletal muscle wasting in cachexia. Here, the role of NF-kappaB in cytokine-induced muscle degeneration was explored. In differentiating C2C12 myocytes, TNF-induced activation of NF-kappaB inhibited SMD by suppressing MyoD mRNA at the posttranscriptional level. In contrast, in differentiated myotubes, TNF plus interferon-gamma (IFN-gamma) signaling was required for NF-kappaB-dependent down-regulation of MyoD and dysfunction of skeletal myofibers. MyoD mRNA was also down-regulated by TNF and IFN-gamma expression in mouse muscle in vivo. These data elucidate a possible mechanism that may underlie the skeletal muscle decay in cachexia.
965 citations
TL;DR: It is shown that MyoD is a DNA binding protein capable of specific interaction with two regions of the mouse muscle creatine kinase gene upstream enhancer, both of which are required for full muscle-specific enhancer activity.
842 citations
TL;DR: Findings indicate that Myod functions in an instructive chromatin context and directly regulates genes that are expressed throughout the myogenic program, achieving promoter-specific regulation of its own binding and activity through a feed-forward mechanism.
Abstract: The expression of Myod is sufficient to convert a fibroblast to a skeletal muscle cell, and, as such, is a model system in developmental biology for studying how a single initiating event can orchestrate a highly complex and predictable response. Recent findings indicate that Myod functions in an instructive chromatin context and directly regulates genes that are expressed throughout the myogenic program, achieving promoter-specific regulation of its own binding and activity through a feed-forward mechanism. These studies are beginning to merge our understanding of how lineage-specific information is encoded in chromatin with how master regulatory factors drive programs of cell differentiation.
758 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2025 | 2 |
| 2024 | 6 |
| 2023 | 7 |
| 2022 | 18 |
| 2021 | 5 |
| 2020 | 2 |