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Study demonstrated that Spry1 has a role in supporting mitogen-induced vascular hyperplasia, at least in part by promoting Akt/Rb signaling and increasing mitogen-induced cyclinD1 expression and decreasing p27Kip1 expression.
SPRY1 maybe a negative feedback regulator in normal human epidermal keratinocytes.
FREM2 is thus proposed as a novel GB biomarker and a putative biomarker of glioblastoma stem cells. Both FREM2 and SPRY1 are expressed on the surface of the GB cells, while SPRY1 alone was found overexpressed in the cytosol of non-malignant astrocytes.
Inhibition of miR-29b could attenuate atherosclerosis by inhibiting the SPRY1/MAPK signaling pathway and inflammation in aorta.
During adipogenesis and osteogenesis, TNF-alpha significantly increased Spry1 levels and overexpression of miR-21 dramatically decreased Spry1 levels in the presence of TNF-alpha, indicated important roles of miR-21 in modulating link between TNF-alpha and Spry1. Our findings introduce a molecular mechanism in which TNF-alpha suppresses adipogenic and osteogenic differentiation of PDLSCs by inhibiting miR-21/Spry1 func...
Although the expression of SPRY1 was low when compared with other tumors, SPRY1 was variably expressed in primary Ewing sarcoma tumors and higher expression levels were significantly associated with improved outcome in a large patient cohort.
SPRY1 and SPRY2 mRNA transcripts were significantly upregulated in human CRC. Suppression of SPRY2 repressed AKT2 and EMT-inducing transcription factors and significantly increased E-cadherin expression. Concurrent downregulation of SPRY1 and SPRY2 also increased E-cadherin and suppressed mesenchymal markers in colon cancer cells.
Spry1 plays a selective role in at least a subset of triple-negative breast cancer to promote the malignant phenotype via enhancing EGF-mediated mesenchymal phenotype.
Suppression of SPRY1 by age-associated methylation inhibits the replenishment of the muscle stem cell pool.
Cosuppression of Sprouty and Sprouty-related negative regulators of FGF signalling in prostate cancer
There is an inverse correlation between the expression of Spry1 and growth, proliferation, invasion and migration of ovarian cancer cells.
A random population of LNCaP prostate cancer cells comprises a heterogeneous group of cells with different androgen-deprivation sensitivities and potential for invasiveness; expression levels of 2 genes known to be regulated by miR-21, an androgen-regulated microRNA, SPRY1 and JAG1 were lower in an androgen insensitive clone, than an androgen sensitive clone.
The Spry1 acts as a sensor of mitogenic activity that not only attenuates RTK signaling but also induces a cellular senescence response to avoid uncontrolled proliferation.
Sprouty1 expression is not connected with mitogenic signaling and cell proliferation.
Spry1 and Spry4 have opposing roles in VSMC phenotypic modulation, and Spry1 maintains the VSMC differentiation phenotype in vitro in part through an Akt/FoxO/myocardin pathway.
Re-expression of SPRY1, a repressed target of BCL11B, limits the transformation capacity of Ewing sarcoma cells.
miR-21 promotes robust fibrogenic EMT of EMCs, in part by directly targeting PDCD4 and SPRY1.
Feedback regulations of miR-21 and MAPKs via Pdcd4 and Spry1 are involved in arsenite-induced cell malignant transformation.
Results suggest that the SPRY1 gene is an important genetic factor for determining the risk of both obesity and osteoporosis in humans.
siRNA-mediated knockdown of Spry1, Spry2, or Spry4 promotes IFN-inducible antileukemic effects in vitro and results in enhanced suppressive effects on malignant hematopoietic progenitors from patients with polycythemia vera.
Results show that Spry1a, 2 and 4 have partially overlapping expression in developing and regenerating Xenopus limbs, which correspond with known areas of Fgf signaling.
Loss of Spry1/2 enhances the survival of effector CD8+ T cells and results in the formation of more protective memory cells. Deleting Spry1/2 in antigen-specific CD8+ T cells may have therapeutic potential for enhancing the survival and functionality of effector and memory CD8+ T cells in vivo.
The results show that lnc-Spry1 could act as an early mediator of TGF-beta signaling and reveal different roles for a long noncoding RNA in modulating transcriptional and posttranscriptional gene expression.
modulation of stromal paracrine signaling and extracellular matrix remodeling by SPRY1 regulates mammary epithelial morphogenesis during postnatal development.
Here, we present a novel mouse model of pheochromocytoma consisting of double-heterozygous mice for Pten and Sprouty1 (Spry1), which leads to pheochromocytomas that appear at earlier onset and grow at a higher rate than those from Pten+/- mice.
Sprouty gain of function disrupts lens cellular processes and growth by restricting receptor tyrosine kinase signaling.
In vivo analysis of thyroid glands from Spry1 knockout mice reveals that Spry1 induces a senescence-associated secretory phenotype via activation of the NFkappaB pathway.
showed that hSpry1 overexpression prevents VEGF secretion
Spry1 and Spry2 coordination is required for normal development of the external genitalia in mice
conjunctival epithelial Spry1 and Spry2 redundantly promote eyelid closure.
Findings demonstrate that Pokemon suppresses Sprouty1 expression through a miR-21-mediated mechanism, affecting the growth and proliferation of liver cancer cells.
ISG15 mRNA expression and IFN-dependent antiviral responses are enhanced in Spry1,2,4 triple knock-out mouse embryonic fibroblasts, consistent with negative feedback regulatory roles for Spry proteins in IFN-mediated signaling.
When Spry1 and Spry2 loss-of-function occurs in the context of heterozygosity for a null allele of the tumor suppressor gene Pten, there is a striking increase in prostatic intraepithelial neoplasia and evidence of neoplastic invasion.
To determine whether modulating RTK signalling may overcome the abnormal nephrogenesis of Fraser syndrome, we introduced a single null Sprouty1 allele into Fras1(bl/bl) mice, reducing the ureteric bud's expression of this anti-branching molecule.
investigation of role of Spry1: Overexpression of Spry1 in transgenic mice leads to lower body fat, reduced bone loss, and normal metabolic function (i.e., prevents liver steatosis/glucose intolerance) compared with Spry1-negative transgenic mice.
findings identify Spry1 as a candidate tumor-suppressor gene in medullary thyroid carcinoma
Studies implicate Spry1 as a novel regulator of erythropoiesis during anemia, transducer of EPO/EPOR signals, and candidate suppressor of Jak2 activity.
SHP2, a major determinant of balance between mESC self-renewal and differentiation, directly regulates Spry1 activity to modulate ERK1/2 signaling and lineage-specific differentiation in mESCs
May function as an antagonist of fibroblast growth factor (FGF) pathways and may negatively modulate respiratory organogenesis.
protein sprouty homolog 1
, sprouty, Drosophila, homolog of, 1 (antagonist of FGF signaling)
, sprouty 1 protein
, sprouty homolog 1, antagonist of FGF signaling (Drosophila)
, sprouty homolog 1, antagonist of FGF signaling
, sprouty 1
, sprouty homolog 1a, antagonist of FGF signaling
, sprouty homolog 1b, antagonist of FGF signaling
, inhibitor of receptor tyrosine kinases