KLF16 antibody - middle region (ARP30079_P050)
- Known as:
- KLF16 (anti-) - middle region (ARP30079_P050)
- Catalog number:
- arp30079_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KLF16 antibody - middle region (ARP30079_P050)
Related genes to: KLF16 antibody - middle region (ARP30079_P050)
- Gene:
- KLF16 NIH gene
- Name:
- Kruppel like factor 16
- Previous symbol:
- -
- Synonyms:
- NSLP2, BTEB4, DRRF
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-27
- Date modifiied:
- 2016-06-03
Related products to: KLF16 antibody - middle region (ARP30079_P050)
Related articles to: KLF16 antibody - middle region (ARP30079_P050)
- Human SERHL, a pseudogene-derived lncRNA, plays a key role in cancer progression. However, the mechanism by which SERHL modulates gastric cancer (GC) is mostly unknown. This study found that SERHL was down-regulated in GC and inversely related to its malignancy. Overexpression of SERHL inhibited cell growth and metastasis in GC cells. Mechanistically, SERHL interacts with KLF16, promoting the degradation of KLF16 via ubiquitination in GC cells. The transcription factor KLF16 binds to the promoters of PLCB1 and PRKCA genes, increasing their expression and enhancing GC invasion and metastasis. SERHL reduces motility by inhibiting the KLF16-PLCB1/PRKCA signaling pathway in GC cells. These results highlight the function and mechanism of SERHL in GC progression, indicating that SERHL has the potential to be a diagnostic marker and therapeutic target in GC. - Source: PubMed
Publication date: 2025/10/20
Hong LinjiePeng SiyangChen YidongXie YanciLei YutingWu JiekeHuang XiaodongWei XiangyangYang PingZhang JiemingYang QiongTang WeimeiWu XiaoshengPeng YingLin ZhizhaoLi AiminLiu SideLi JiayingDai WeiyuWang Jide - The Kruppel-like factor (KLF) family comprises transcription factors that share conserved zinc-finger domains and orchestrate key pathophysiological processes in the liver, including glucose and lipid metabolism, inflammatory responses, and fibrogenesis. In this review, we systematically dissect the roles of major KLF members-specifically KLF2-KLF10, KLF14, KLF15, and KLF16-in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD), liver fibrosis/cirrhosis, and hepatocellular carcinoma (HCC). We discuss several key findings. First, KLF16 drives fatty acid β-oxidation by activating peroxisome proliferator-activated receptor alpha (PPARα), whereas KLF4 and KLF2 suppress lipogenesis through the inhibition of SREBP-1c. Second, with respect to hepatic stellate cell activation, KLF6 and KLF5 promote fibrogenesis, whereas KLF14 has anti-fibrotic effects through the upregulation of peroxisome proliferator-activated receptor gamma (PPARγ). Third, in HCC, KLF2, KLF4, and KLF6 act as tumour suppressors, and are frequently epigenetically silenced, whereas KLF5, KLF7, and KLF8 function as oncogene products, by modulating Wnt/β-catenin signaling, glycolysis, and immune evasion. Last, emerging modalities, such as proteolysis-targeting chimeras and cell type-specific nanoparticle delivery, are described. These represent potential new avenues for KLF-targeting therapy. By delineating these context-dependent mechanisms, we provide a theoretical framework for the development of KLF-based precision strategies for the treatment of major liver diseases. - Source: PubMed
Publication date: 2026/06/25
Chen HepuHuang ShushengZhou ZhigangLi JialinPeng QingTu Jian - Programmed death ligand 1 (PD-L1)-driven immune escape is a crucial mechanism in the progression of hepatocellular carcinoma (HCC). Furthermore, Krüppel-like factor 16 (KLF16) may be a key molecule that regulates this process. Therefore, the role of KLF16 in PD-L1-driven immune escape in HCC was investigated. - Source: PubMed
Publication date: 2026/07/20
Kong ShujiaZhao ChenLu FangyiLi Yanwen - Polycystic ovary syndrome (PCOS) frequently co-occurs with obesity, insulin resistance, dyslipidaemia and metabolic syndrome (MetS). However, whether this metabolic burden represents secondary comorbidity or an intrinsic component of PCOS genetic architecture remains unclear. - Source: PubMed
Publication date: 2026/07/01
Wang SuijianWang Kui - Despite antiretroviral therapy, human immunodeficiency virus type 1 (HIV-1) persists in latently-infected cells through epigenetic and transcriptional mechanisms. Latency-reversing agents have failed clinically, partly due to incomplete understanding of HIV-1 latency reversal. Here, using DNA-affinity capture and mass spectrometry on the HIV-1 5' long terminal repeat (5'LTR) enhancer-core promoter, we identify KLF16 (Krüppel-like Factor 16) as a novel regulator of HIV-1 gene expression. KLF16 binds to the HIV-1 5'LTR at Sp1 binding sites, and KLF16 depletion reactivates latent HIV-1 in T-lymphoid and monocytic cell models. Mechanistically, KLF16 represses HIV-1 transcription by competing with Sp1 for promoter binding and by recruiting the Sin3A/HDAC1 and HP1α/Suv39H1 repressive epigenetic complexes. KLF16 is also upregulated in CD4 T cells from ART-treated people with HIV-1 upon T-cell activation. Additionally, All-Trans retinoic acid (ATRA) reactivates latent HIV-1 in myeloid cells, partly by downregulating KLF16. These findings establish KLF16 as a novel transcriptional repressor of HIV-1, identifying it as a potential promising therapeutic target for cure strategies. - Source: PubMed
Publication date: 2026/06/04
Santangelo MarionBendoumou MaryamDutilleul AntoineKhalfi SoumiaPlant EstelleNgassaki-Yoka Christ DominiquePilosio LisaVanhulle CarolineDias JonathanMarray TristanFattaccioli AntoineVerhasselt BrunoLange UlrikeDieu MarcRouty Jean-PierreRohr OlivierRenard PatriciaAncuta PetronelaVAN Lint Carine