Редактирование: ZFP36L1

mRNA decay activator protein ZFP36L1 (Butyrate response factor 1) (EGF-response factor 1) (ERF-1) (TPA-induced sequence 11b) (Zinc finger protein 36, C3H1 type-like 1) (ZFP36-like 1) [BERG36] [BRF1] [ERF1] [RNF162B] [TIS11B]

==Publications==

{{medline-entry
|title=Zinc finger protein [[ZFP36L1]] promotes osteoblastic differentiation but represses adipogenic differentiation of mouse multipotent cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28206953
|abstract=Zinc finger protein 36, C3H type-like 1 ([[ZFP36L1]]) is a member of the tristetraprolin (TTP) family and its role in the aging-related bone loss is currently unknown. We present evidence that [[ZFP36L1]] expression in rat femurs and bone marrow mesenchymal stem cells (bmMSCs) was down-regulated with aging. [[ZFP36L1]] knockdown decreased osteoblastic differentiation of MC3T3-E1 and C3H10T1/2 cells, and increased adipogenic differentiation of 3T3-L1 and C3H10T1/2 cells, whereas [[ZFP36L1]] overexpression did the opposite. The finding that [[ZFP36L1]] overexpression enhanced osteoblastic and repressed adipogenic differentiation was also corroborated by ex vivo experiments. Troglitazone prevented [[ZFP36L1]] from inhibiting adipogenic differentiation, suggesting the significance of PPARγ2 repression in [[ZFP36L1]]'s inhibitory effect on adipogenic differentiation. [[ZFP36L1]] overexpression repressed the expression of Pparγ2 mRNA, but not the PPARγ promoter activity. Biotin pull-down and electrophoretic mobility-shift assays suggested that [[ZFP36L1]] might interact with endogenous Pparγ2 mRNA by binding to its 3'UTR. The [[ZFP36L1]]-containing ribonucleoprotein complexes of [[ZFP36L1]]-overexpressing cells contained less Pparγ2 mRNA than those of control cells. In a luciferase reporter construct, replacement of the SV40 poly(A) fragment by the 3'UTR of Pparγ2 mRNA reduced the expression of luciferase transcripts in [[ZFP36L1]]-overexpressing cells. Examination of the kinetic expression of Pparγ2 mRNA after transcriptional blockage showed that [[ZFP36L1]] might enhance the degradation of the transcripts. Together, these data imply that [[ZFP36L1]] overexpression might repress adipogenesis at least by down-regulating PPARγ2 expression through post-transcriptional mechanisms. Thus, our findings support the notion that decrease of [[ZFP36L1]] expression in bmMSCs with aging might contribute to the aging-related bone loss.
|mesh-terms=* Adipocytes
* Aging
* Animals
* Blotting, Western
* Butyrate Response Factor 1
* Cell Differentiation
* Electrophoretic Mobility Shift Assay
* Gene Expression Regulation
* Immunoprecipitation
* Mice
* Multipotent Stem Cells
* Nuclear Proteins
* Osteoblasts
* Osteoporosis
* RNA-Binding Proteins
* Rats
* Real-Time Polymerase Chain Reaction
|keywords=* Gerotarget
* ZFP36L1
* adipogenesis
* aging-related bone loss
* osteoblastogenesis
* osteoporosis
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5400528
}}