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Serine-threonine Kinase, ROCK2, Regulates Germinal Center B Cell Positioning and Cholesterol Biosynthesis

ABSTRACT: Serine-threonine Kinase, ROCK2, Regulates Germinal Center B Cell Positioning and Cholesterol Biosynthesis

PROVIDER: PRJNA593194 | ENA |

REPOSITORIES: ENA

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Serine-threonine Kinase, ROCK2, Regulates Germinal Center B Cell Positioning and Cholesterol Biosynthesis

Project description:Splenic follicular B cells (FoB; B220+GL7-CD38hiCD23+) and Germinal Center B cells (GCB; B220+GL7+CD38lo) were FACS sorted from WT or CD23-Cre.Rock2 mice after 7d post-immunization with NP-CGG. RNA-seq was then employed to compare the transcriptome of GCBs from the indicated mice. Here we show that loss of ROCK2 leads to altered gene expression in GCBs. We also employed ATAC-seq analysis and found that differentially expressed genes from the ROCK2-deficient GC B cells contained loci that were enriched for IRF binding sites.

2020-05-22 | GSE141328 | GEO

Serine-threonine kinase ROCK2 regulates germinal center B cell positioning and cholesterol biosynthesis.

Project description: Not available

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Transcription profiling of mouse NIH3T3 cells over-expressing RNA-dependent serine/threonine protein kinase (PKR)PKR

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Serine/Threonine phosphatase PP2A is essential for optimal B cell function

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PrrA modulation of Mycobacterium tuberculosis response to acidic pH and high chloride levels is critically regulated by serine/threonine protein kinases

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Oncogenic Serine-Threonine Kinase Receptor Associated Protein Supports Hepatocellular Carcinoma Cell Growth by Enhancing Wnt/β-catenin Signaling

Project description:Serine-threonine kinase receptor-associated protein (STRAP) is upregulated in breast, colorectal and lung cancers, promoting their growth. We identify the upregulation of STRAP in hepatocellular carcinomas. Elevated STRAP endows tumor cells with growth advantage by reprograming a variety of metabolic processes and signaling pathways critical for hepatocellular carcinoma progression. Especially, enhanced Wnt/β-catenin signaling is likely to be a major effector of its tumor-promoting role.

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Serine/Threonine phosphatase PP2A is essential for optimal B cell function

Project description:Protein phosphatase 2A (PP2A), a serine/threonine phosphatase, has been shown to control T cell function. We found that in vitro activated B cells and B cells from various lupus-prone mice and patients with systemic lupus erythematosus display increased PP2A activity. To understand the contribution of PP2A to B cell function, we generated a Cd19CrePpp2r1aflox/flox (flox/flox) mouse which lacks functional PP2A only in B cells. Flox/flox mice displayed reduced spontaneous germinal center formation and decreased responses to T-dependent and T-independent antigens while their B cells responded poorly in vitro to stimulation with an anti-CD40 antibody or CpG in the presence of IL-4. Transcriptome and metabolome studies revealed altered NAD and purine/pyrimidine metabolism and increased expression of purine nucleoside phosphorylase in PP2A-deficient B cells. Our results demonstrate that PP2A is required for optimal B cell function and may contribute to increased B cell activity in systemic autoimmunity.

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Inhibition of Rho-associated, coiled-coil-containing protein kinase 2 in murine podocytes

Project description:Focal segmental glomerulosclerosis (FSGS) is characterized by damage to podocytes, a crucial pathological feature. While several mechanisms of podocyte injury have been suggested, many questions remain unanswered. Rho-associated, coiled-coil-containing protein kinase 2 (ROCK2), a serine/threonine kinase with diverse cellular functions, appears to play a significant role. We observed activation of ROCK2 in podocytes of mice with FSGS induced by adriamycin (ADR), as well as in cultured podocytes exposed to ADR. To delve deeper, we used conditional knockout mice where the ROCK2 gene was specifically disrupted in podocytes (PR2KO). These mice showed resistance to ADR-induced albuminuria, glomerular sclerosis, and podocyte damage. Additionally, pharmacological inhibition of ROCK2 significantly improved podocyte loss and kidney sclerosis in a mouse model of FSGS by counteracting profibrotic factors. RNA sequencing of podocytes treated with a ROCK2 inhibitor confirmed ROCK2's role as a regulator of the cyclic nucleotide signaling pathway. Our findings underscore the potential of ROCK2 inhibition as a therapeutic avenue for FSGS.

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