Ask about this productRelated genes to: ZFP36L2 antibody
- Gene:
- ZFP36L2 NIH gene
- Name:
- ZFP36 ring finger protein like 2
- Previous symbol:
- BRF2
- Synonyms:
- ERF2, RNF162C, TIS11D
- Chromosome:
- 2p21
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-09
- Date modifiied:
- 2016-10-05
Related products to: ZFP36L2 antibody
Related articles to: ZFP36L2 antibody
- - Source: PubMed
Publication date: 2026/04/20
Wang JiaxueSong JingyanChen WenLiang QihuiWu HaicuiGuan LuLian Fang - RNA-binding proteins, Zinc Finger Protein 36-Like 1 (ZFP36L1) and Zinc Finger Protein 36-Like 2 (ZFP36L2), post-transcriptionally regulate the expression of a large number of genes involved in various cellular processes. However, specific or redundant functions of ZFP36L1 and ZFP36L2 in liver homeostasis have never been explored. Here, we hypothesized that ZFP36L1 and ZFP36L2 are functionally redundant in the liver, and their combined deficiency would stabilize their direct mRNA targets, which would alter liver homeostasis. - Source: PubMed
Publication date: 2026/04/17
Kumar RahulBlackshear Perry JPatial SonikaSaini Yogesh - Zinc-finger protein 36 (Zfp36) family RNA-binding proteins such as tristetraprolin (TTP/Zfp36), butyrate response factor (BRF)-1/Zfp36L1, and BRF-2/Zfp36L2, regulate the expression of cytokine/chemokine mRNA with AU-rich elements. In traumatic brain injury (TBI), reactive astrocytes produce various cytokines and chemokines that induce neuroinflammation. However, despite their importance in neuroinflammation, little is known about the regulation of cytokine and chemokine production by the Zfp36 family proteins in astrocytes. Endothelin-1 (ET-1), which promotes the conversion to reactive astrocytes, stimulates astrocytic cytokine and chemokine production. In the present study, we examined the effects of ET-1 on Zfp36 family protein expression in astrocytes and the roles of these proteins in cytokine/chemokine production. ET-1 (100 nM) increased the expression of TTP and BRF-1 in cultured astrocytes. In a mouse model of TBI, TTP and BRF-1 expression increased, which was reduced by intracerebroventricular administration of BQ788, an ET antagonist. Immunohistochemical analyses showed that TTP and BRF-1 were present in reactive astrocytes. Knockdown of TTP by siRNA enhanced the production of ET-induced CCL2 and IL-6 in cultured astrocytes, while BRF-1 knockdown enhanced the CCL2, CXCL1 and CX3CL1 production. RNA immunoprecipitation/PCR analyses showed that ET-1 stimulated TTP binding to CCL2 and IL-6 mRNAs, and BRF-1 binding to CCL2, CXCL1 and CX3CL1 mRNAs. These results suggest that ET-1 stimulates the induction of TTP and BRF-1 in astrocytes, and that the production of some astrocytic chemokine/cytokine is negatively regulated by the increments in TTP and BRF-1 production. - Source: PubMed
Publication date: 2026/04/02
Koyama YutakaNishiuma AinaTakahashi NagiIzumikawa EriHamada ChisatoIzumi YasuhikoHishinuma ShigeruMichinaga Shotaro - Type I interferons restrict HIV-1 replication by inducing antiviral genes, but the full spectrum of their effectors remains incompletely defined. Here we identify ZFP36L2, a nuclear RNA-binding protein, as an IFN-β-induced inhibitor of HIV-1 infection. Silencing of ZFP36L2 impairs IFN-β-mediated HIV-1 inhibition, whereas overexpression of ZFP36L2 suppresses viral replication. Notably, reconstitution of ZFP36L2 in CD4⁺ T cells from HIV-1-infected individuals reduces viral spread ex vivo, and ZFP36L2 transcript levels inversely correlate with plasma viral loads in vivo. Mechanistically, ZFP36L2 binds to the HIV-1 Rev protein and inhibits the nuclear export of Rev response element-containing viral transcripts, thereby blocking downstream viral protein expression. A Rev mutant lacking amino acids 109-116 fails to bind ZFP36L2 and exhibits resistance to ZFP36L2-mediated inhibition, underscoring the functional significance of this interaction. These findings establish ZFP36L2 as an IFN-β-induced antiviral factor that suppresses HIV-1 replication through Rev-dependent inhibition of viral RNA export. - Source: PubMed
Publication date: 2026/04/03
Pang HailinCui HualuYin XiaowanYang ZengwenShang HongLiang Guoxin - The thymus is a primary lymphoid organ in which diverse and self-tolerant T cells are produced from bone marrow-derived hematopoietic progenitors. Progressive, age-associated thymic involution reduces T-cell output and impairs adaptive immunity; however, the molecular mechanisms underlying this process remain elusive. Here, we report that the conditional deletion of the RNA-binding proteins Zfp36l1 and Zfp36l2 in thymic epithelial cells (TECs) leads to a pronounced reduction in the number of TECs during the embryonic stage and early neonatal stage, despite a largely preserved thymus size. Postnatally, these mice exhibit excessive medullary TEC (mTEC) expansion, elevated intrathymic proinflammatory cytokine production, FOXN1 downregulation, and premature thymic involution. These findings reveal a protective role for Zfp36 Tristetraprolin (TTP) family proteins in regulating cytokine levels within the thymic microenvironment and preventing premature thymic involution. Moreover, our results suggest a previously unappreciated connection between central tolerance induction and the onset of age-associated thymic involution. - Source: PubMed
Publication date: 2026/03/16
Han JianxunGolzari-Sorkheh MahdiehRajan VinothkumarZúñiga-Pflücker Juan Carlos