In this study, we identify and characterize the promoter of the mouse Gas6 gene, a negative regulator of chondrogenic differentiation. We identified two highly conserved regions within the core Gas6 promoter, which are conserved among mouse, human, and rat Gas6 genes, named A-BOX and B-BOX. Basal transcriptional activity was significantly reduced after deletion of either the A-BOX or the latter half of the B-BOX. After treatment with BMP-2 for 3 days, putative A-BOX Binding Factor(s) B (ABFB) and B-BOX Binding Factor(s) (BBF) were unable to bind to their specific motifs in C3H10T1/2 cells, compared with untreated control cells. In addition, we confirmed binding of an NF-Y site within the core promoter region of mouse Gas6 gene. Taken together, these observations provide insight into the mechanism by which Gas6 is downregulated during mesenchymal stem cells differentiation into chondrocytes.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bbrc.2008.04.130DOI Listing

Publication Analysis

Top Keywords

mouse gas6
12
gas6 promoter
8
gas6 gene
8
binding factors
8
gas6
6
identification characterization
4
mouse
4
characterization mouse
4
promoter
4
promoter study
4

Similar Publications

PGAM5 and VDAC1 have both been reported to regulate mitophagy. However, the mechanisms by which they regulate sepsis-induced inflammatory microvascular injury remain unverified. In previous studies, we established the role of this regulatory axis in various phenotypic processes, including mitophagy, mitochondrial biogenesis, the mitochondrial unfolded protein response, and mitochondrial dynamics, while further confirming the interactive regulatory proteins within this axis.

View Article and Find Full Text PDF

Background: Neuropathic pain (NPP) is a multifaceted pain syndrome that occurs as a consequence of physical injury or underlying diseases, with an incidence rate of 7%-10%, NPP poses a significant clinical challenge as current treatment options are ineffective. The accumulation of apoptotic cells and neuroinflammation play crucial roles in the pathological mechanisms of NPP. Here, we aim to investigate strategies for effectively clearing apoptotic cells and provide therapeutic interventions for NPP.

View Article and Find Full Text PDF

Background: Psychological stress can exacerbate the development of allergies; however, the underlying mechanisms remain poorly understood. IgE-mediated cutaneous allergic inflammation (IgE-CAI) is a basophil-dependent skin allergy with eosinophil infiltration at inflammatory sites. Its resolution involves anti-inflammatory programmed death ligand 2 (PD-L2)-positive macrophages.

View Article and Find Full Text PDF

AXL/GAS6 signaling governs differentiation of tumor-associated macrophages in breast cancer.

Exp Cell Res

January 2025

Immunology Laboratory, Department of Zoology, University of Calcutta, 35, Ballygunge Circular Road, Kolkata, 700019, West Bengal, India. Electronic address:

Most epithelial cancers are infiltrated by prognostically relevant myelomonocytic cells. Immunosuppressive tumor associated macrophages (TAMs) and their precursor monocytic myeloid-derived suppressor cells (MDSCs) have previously been associated with worse outcomes in human breast cancer (BCa), yet the mechanism of immunosuppressive TAMs-polarization from myelomonocytic precursors is not completely understood. In this study, we show that persuaded AXL/GAS6 pathway alters macrophage phenotype from HLA-DRCD206CD163 classical phagocytic into HLA-DRCD206CD163 immunosuppressive ones with accelerated BCa progression, and increased angiogenesis signature and invasion ability of cancer cells at tumor beds.

View Article and Find Full Text PDF

As catabolic enzyme, CD73 dephosphorylates adenosine monophosphate (AMP) and can also regulate tumor cell proliferation and metastasis. To date, very few studies have explored the role of CD73 in mediating non-small cell lung cancer (NSCLC) metastasis, and the underlying transducing signal has not been elucidated. In the present study, we demonstrated that the CD73/Axl axis could regulate Smad3-induced epithelial-to-mesenchymal transition (EMT) to promote NSCLC metastasis.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!