KLF6 antibody - N-terminal region (ARP35640_P050)
- Known as:
- KLF6 (anti-) - N-terminal region (ARP35640_P050)
- Catalog number:
- arp35640_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KLF6 antibody - N-terminal region (ARP35640_P050)
Ask about this productRelated genes to: KLF6 antibody - N-terminal region (ARP35640_P050)
- Gene:
- KLF6 NIH gene
- Name:
- Kruppel like factor 6
- Previous symbol:
- BCD1, ST12, COPEB
- Synonyms:
- CPBP, GBF, Zf9, PAC1
- Chromosome:
- 10p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-16
- Date modifiied:
- 2016-10-05
Related products to: KLF6 antibody - N-terminal region (ARP35640_P050)
Related articles to: KLF6 antibody - N-terminal region (ARP35640_P050)
- Estrogen deficiency results in enhanced bone resorption by osteoclasts, a critical factor in the development of postmenopausal osteoporosis. This study investigates the regulatory role of KLF6 in osteoclast differentiation and evaluates its potential in reducing bone loss in ovariectomized (OVX) mice. The results show that the expression of KLF6 gradually decreases during osteoclast differentiation, and this decrease is more pronounced in the OVX model. Reducing the expression level of KLF6 can promote the differentiation of osteoclasts. Through RNA sequencing and ChIP analysis, we found that KLF6 inhibits the activity of the MAPK signaling pathway by upregulating the expression of DUSP16, thereby suppressing osteoclast differentiation. In vivo experiments demonstrate that overexpression of KLF6 via adeno-associated virus can reduce OVX-induced bone loss, suggesting that KLF6 may serve as a potential therapeutic target for bone loss caused by estrogen deficiency. - Source: PubMed
Publication date: 2026/03/28
Yang ChenZhang WeiLiu XinLi WenmingQin YiLi WenhaoWu ZebinJiang KunlongWang ChenglongQian ZhonglaiWang LiangliangGeng Dechun - is indispensable for hematopoiesis, with knockout mice typically exhibiting embryonic lethality attributed to severe anemia and defective hematopoietic stem cell (HSC) development. Intriguingly, we obtained viable adult mice harboring a 17-nucleotide deletion in exon 2, which displayed intact T-cell development despite a significantly reduced bone marrow HSC pool. While mutant HSCs exhibited attenuated lymphoid potential, they retained partial myeloid reconstitution capacity. Single-cell transcriptomic analysis revealed compensatory upregulation of key hematopoietic regulators, including and , in -deficient HSCs. Comprehensive profiling further demonstrated preservation of the complete T-cell hierarchy, including all major subsets, in mutant mice. These findings provide evidence that knockout mice may be viable, and T-cell development may proceed independently of definitive hematopoiesis. - Source: PubMed
Publication date: 2026/05/22
Li YuhangDang ShiyingLi JinbingZhang TianDu JuanPan GuangjinHuang Ke - Fucosyltransferase 8 (FUT8)-mediated core fucosylation (CF) has been confirmed to regulate multiple disease progression. However, its role in myocardial ischaemia/reperfusion (I/R) injury are unclear. - Source: PubMed
Publication date: 2026/06/04
Peng HaiyanZhang HangHu ZheXiao BinlanLi YuanmaoJiang Zhenzhu - Early life is essential for establishing memory T cells, which rapidly populate mucosal sites during infancy, although these nascent memory T cells are less protective than their adult counterparts. Here we used single-cell RNA sequencing of resting and CD3+CD28 antibody-stimulated T cells from lymphoid and mucosal tissues of infant (2-9 months) and adult (40-63 years) organ donors to investigate age-dependent mechanisms for functional regulation of human memory T cells. Infant CCL5 effector memory T cells exhibited reduced effector function compared to adults. Transcription factor network analysis identified HELIOS and KLF6 as regulators of memory T cell states in infant and adult tissues, respectively. Using single-nucleus RNA sequencing, assay for transposase-accessible chromatin sequencing and CRISPR-Cas9 knockout, we defined HELIOS (IKZF2) as a critical regulator of the infant-specific transcriptional program in CCL5 effector memory T cells and restricted effector function in SELLCCR7 naive and/or central memory T cells. Our findings reveal key mechanisms controlling T cell functional states in early life. - Source: PubMed
Publication date: 2026/06/02
Szabo Peter ALevitin Hanna MNargund SiddhiConnors Thomas JChen DavidJin JennyThapa PuspaGuyer RebeccaCaron Daniel PGray Joshua IMatsumoto ReiKubota MasaruBrusko MaiganBrusko Todd MFarber Donna LSims Peter A - Inflammatory response-related signaling pathways are associated with Atherosclerosis (AS), yet the particular inflammation-related genes underpinning this process are still not fully characterized. - Source: PubMed
Publication date: 2026/05/20
Xu XuJiang MeilingHuang ZeyunZhu Guofu