ZFP36L1 antibody - N-terminal region (ARP33382_P050)
- Known as:
- ZFP36L1 (anti-) - N-terminal region (ARP33382_P050)
- Catalog number:
- arp33382_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZFP36L1 antibody - N-terminal region (ARP33382_P050)
Related genes to: ZFP36L1 antibody - N-terminal region (ARP33382_P050)
- Gene:
- ZFP36L1 NIH gene
- Name:
- ZFP36 ring finger protein like 1
- Previous symbol:
- BRF1
- Synonyms:
- RNF162B, Berg36, ERF1, TIS11B, cMG1
- Chromosome:
- 14q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-09
- Date modifiied:
- 2016-06-30
Related products to: ZFP36L1 antibody - N-terminal region (ARP33382_P050)
Related articles to: ZFP36L1 antibody - N-terminal region (ARP33382_P050)
- 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 - Genetic background is a major determinant of disc degeneration, a leading cause of chronic back pain and disability. Herein, we demonstrate that premature disc cell senescence contributes to early-onset degeneration in SM/J mice and test two systemic senotherapeutic strategies to mitigate it: Navitoclax (Nav.) and a cocktail of Dasatinib and Quercetin (DQ). While Nav. treatment did not improve severe degeneration in SM/J mice or senescence status, DQ-treated mice showed lower grades of degeneration and a decreased abundance of senescence markers, including p19ARF, p21, and the senescence-associated secretory phenotype (SASP). DQ improved disc cell viability and phenotype retention and retarded fibrosis of the nucleus pulposus tissue. Transcriptomic analysis revealed tissue-specific effects of the treatment, with cell cycle regulation and JNK signaling being commonly affected across different tissue types. A comparison of SM/J data with DQ-mediated aging-dependent amelioration of disc degeneration in C57BL/6 N mice identified Junb and Zfp36l1 signaling as shared DQ targets in the mouse disc. Notably, the in vitro inhibition studies of the JUN pathway in human degenerated NP cells mimicked the benefits of DQ, namely, a reduction in senescence and SASP. This study reinforces the efficacy of senolytic treatment in ameliorating local senescence and intervertebral disc fibrosis. - Source: PubMed
Publication date: 2026/04/14
Novais Emanuel JOttone Olivia KJagannath SanjanaAkande Esther JesutofunmiBarve Ruteja ARisbud Makarand V - 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 - Keratoconus (KC) is a degenerative corneal disease with a complex etiology that severely affects vision. Butyrate is a saturated short-chain fatty acid with anti-inflammatory properties. Accumulating evidence underscores a significant role for inflammation in KC pathogenesis. However, the specific role of butyrate metabolism in KC remained unclear. This study aimed to identify key genes associated with butyrate-related regulatory pathways in KC. - Source: PubMed
Publication date: 2026/04/02
Gao NaHuang HuiTian YuHu JiachunWang WanjieYe HejiangDong Xiaojuan - Non-small cell lung cancer (NSCLC) is the predominant lung cancer subtype with high mortality rate. Drug resistance and immune evasion limit its therapeutic outcomes. Specific mechanism of the oncogenic ZFP36L1 in NSCLC remains unclear. - Source: PubMed
Wang LijieChen BiaoHe JinxianLin ChengbinShen WeiyuLv WangWang LumingHu Jian