Project description:The scavenger receptor CD36 plays critical roles in lipid uptake and triggering of inflammatory response, via activation of guanine nucleotide exchange factor Vav. We used microarrays to detail the different up-regulated or down-regulate genes among three vav familymembers.
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to evaluate the gene expression of E4BP4 knockout (KO) RAW264.7 cells. Methods: We generated E4BP4-KO RAW264.7 Cell Line using CRISPR-CAS9 system. Control plasmid was encoding the Cas9 nuclease without gRNA sequence. Total RNA of E4BP4-KO and Control (CTRL) RAW264.7 cells was extracted. RAW264.7 cells RNA profiles were generated by deep sequencing for two groups (E4BP4-KO versus CTRL RAW264.7 cells) with three samples each. Results: There were significant differences between E4BP4-KO and CTRL RAW264.7 cells. Conclusions: Deletion of E4BP4 in RAW264.7 cells induced various changes at the transcription level.
Project description:Gfi1 is a transcription factor broadly participate in differentiation of immune cells and loss of Gfi1 could result in severe neutrophil deficiency. To gain insight into the consequences of lack of Gfi1 on a genome-wide level, we conducted genome-wide transcriptome profiling in Wide-type (WT) and Gfi1–/– Raw264.7 macrophage cells using Affymetrix Mouse 3’ IVT microarrays
Project description:In sepsis, infection and immunosuppression occur simultaneously. We currently found that Samsn1 expression is increased on myeloid cells in sepsis. And, Samsn1 is currently recognized as a negative regulator of immune response. So we constructed Samsn1 knockout Raw264.7 cells to study the effect of Samsn1 on macrophage function and the gene expression of macrophages with infection.
Project description:Here, we report that the Rho GTPase activators Vav2 and Vav3 utilize a new, miR-200c-dependent mechanism that maintains the epithelial state by limiting the abundance of the Zeb2 transcriptional repressor in breast cancer cells. In parallel, Vav proteins engage an expression program that maintains epithelial cell traits in 3D culture. Depletion of Vav proteins triggers EMT in epithelioid breast cancer cells and, conversely, expression of constitutively active Vav2 restores both miR-200c expression and epithelial traits in mesenchymal breast cancer cells. In silico analyses suggest that the negative Vav-Zeb2 axis is operative in human luminal breast tumors.
Project description:Cutaneous squamous tumors rely on autocrine/paracrine loops for proper fitness. Targeting this Achilles’ heel is therefore considered a potential avenue for patient treatment. However, the mechanisms that engage and sustain such programs during tumor ontogeny are poorly understood. Here, we show that two Rho/Rac activators, the exchange factors Vav2 and Vav3, control the expression of an epithelial autocrine/paracrine program that regulates keratinocyte survival and proliferation as well as the creation of an inflammatory microenvironment. Vav proteins are also critically involved in some of the subsequent autocrine signaling loops activated in keratinocytes. The genetic inactivation of both Vav proteins reduces tumor multiplicity without hampering skin homeostasis, thus suggesting that pan-specific Vav therapies may be useful in skin tumor prevention and treatment.
