Ask about this productRelated genes to: NELFB antibody
- Gene:
- NELFB NIH gene
- Name:
- negative elongation factor complex member B
- Previous symbol:
- COBRA1
- Synonyms:
- KIAA1182, NELF-B
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 2008-02-21
- Date modifiied:
- 2016-10-05
Related products to: NELFB antibody
Related articles to: NELFB antibody
- Emerging evidence suggests that gut microbiota-derived signals can influence distant organs including the skeleton, yet the key microbial effectors remain elusive. Here, we identify Amuc_1473, a previously uncharacterized protein enriched in extracellular vesicles (EVs) from the commensal bacterium Akkermansia muciniphila (Akk), as a critical mediator of gut-bone communication. Amuc_1473 directly promotes osteogenesis and suppresses osteoclastogenesis by binding to negative elongation factor E (NELF-E) and ribosomal protein L26 (RPL26), regulators of transcriptional pausing and mRNA translation, respectively. Notably, Amuc_1473 levels decline in bone and circulation under diverse pro-osteoporotic conditions-including aging, estrogen deficiency, mechanical unloading, high-fat diet, smoking, alcohol, and chronic stress-paralleling reductions in Akk and its EVs. Intermittent fasting robustly restores Akk abundance, Amuc_1473 levels, and bone quality in these models, via enhanced mucin production. Our findings establish Amuc_1473 as a microbial effector that systemically regulates bone homeostasis, offering a translatable strategy to prevent or treat multifactorial osteoporosis. - Source: PubMed
Publication date: 2026/06/13
Rao Shan-ShanZeng Hai-JinWang ZunHong Chun-GuTan Yi-JuanDuan Yan-XinLuo Jing-YaoLuo Ming-JieLiu Yi-WeiWang XinLuo YiWan Teng-FeiZhou YongWang Zheng-GuangHu Guo-WenYin HaoHu Xin-YueWang Zhen-XingHe Ze-HuiCheng Si-YiDu WeiGuan ZheLang Hai-LiLiu Hong-JiCao JiaChen PengLiu Jiang-HuaXie HuiChen Chun-Yuan - In mammals, meiotic silencing of unsynapsed chromatin (MSUC) is initiated by the DNA damage response (DDR) pathway, as marked by γH2AX. During normal male meiosis, MSUC is restricted to the unsynapsed sex chromosomes, a process known as meiotic sex chromosome inactivation (MSCI). While the initiation of MSCI has been well studied, its full silencing dynamics and underlying structural mechanisms remain unclear. In contrast to MSCI, broader MSUC can occur on autosomes in response to synapsis failure, but its cell-to-cell variability obscures its quantification. To address these challenges, we introduce "digital-chromosome-banding", a single-cell-based approach that allows quantitative analysis of MSCI and MSUC at chromosomal resolution. Using this approach, we identified two distinct silencing transitions during MSCI, occurring from zygonema to early pachynema and from early to mid-pachynema. The latter step coincides with mature sex body formation and involves a gel-like diffusion barrier to enforce transcriptional repression. Applying this approach to synapsis-defective mouse models ( , cKO, and cKO), we observed divergent MSUC patterns that correlate with the severity of asynapsis. Comparative analysis between sexes also uncovered notable sexual dimorphisms in meiotic silencing. Together, our data provide a quantitative framework to dissect the spatiotemporal dynamics and sexual differences of meiotic silencing. - Source: PubMed
Publication date: 2026/06/01
Peng YihengWang ShuangqiShrestha RoyalTian XingZakharchenko EvanMaezawa SoAscencao CarollineSmolka MarcusCohen PaulaReddi Prabhakara PoothiNamekawa Satoshi HQiao Huanyu - Metazoan RNA polymerase II is prone to pause in the promoter-proximal region of genes. This pausing involves DRB Sensitivity-Inducing Factor (DSIF) and Negative Elongation Factor (NELF). DSIF and NELF, however, are insufficient to fully reconstitute the degree of promoter-proximal pausing observed in cells. Their negative effects are counteracted by transcription initiation factor TFIIF or by physiological nucleotide concentrations, indicating an additional factor is required. Here, we report that Elongation Factor Homolog 1 (ELOF1) is this missing factor. ELOF1 is enriched in the promoter-proximal region of genes, and its rapid degradation reduces pause duration in cells. In reconstituted assays, ELOF1 potently enhances pausing induced by DSIF and NELF at physiological nucleotide concentrations. Cryo-EM structures reveal that DSIF-NELF-ELOF1 sterically clashes with the position of TFIIF on RNA polymerase II. Accordingly, RNA polymerase II-DSIF-NELF-ELOF1, but not RNA polymerase II-DSIF-NELF, counteracts the positive effects of TFIIF. Our results establish ELOF1 as a core component of promoter-proximal paused RNA polymerase II. - Source: PubMed
Publication date: 2026/05/28
Vazquez Nunez Roberto JBressin AnnkatrinShao ZhihaoMayer AndreasVos Seychelle M - Regulation of adipogenesis has classically been viewed through the lens of transcription initiation driven by lineage defining transcription factors. In this study, we uncover transcription elongation as a critical and previously underappreciated regulatory layer controlling adipocyte cell fate. We demonstrate that the elongation factors Spt4 and Spt6 are indispensable for adipogenic differentiation, as their depletion severely impairs adipogenic gene induction and perilipin expression. Spt4 and Spt6 directly regulate the genes coding for core adipogenic transcription factors, including , , , and , by promoting RNA polymerase II (Pol II) progression through their gene bodies. In the absence of these factors, Pol II becomes stalled at the transcriptional start sites of these adipogenic genes. These data support a post transcription initiation requirement for Spt4 and Spt6 in productive elongation rather than promoter loading. Our findings identify transcription elongation control as a key determinant of adipogenic fate. - Source: PubMed
Publication date: 2026/03/27
Gomez JulianMahapatra SamikshaBatzorig UyangaLiu YeFernández-Méndez CeliaQuadir NehaSen George L - Regulation of RNA polymerase II (Pol II) transcription is closely associated with cell proliferation. However, it remains unclear how the Pol II transcription program is rewired in cancer to promote uncontrolled growth. Here, we find that expression of NELFCD, a known negative transcription elongation factor, is upregulated in colorectal tumors. Auxin-dependent protein degradation of NELF-C in combination with nascent transcript sequencing demonstrates a direct role of NELF-C on Pol II transcription in this cancer. Strikingly, we demonstrate that the acute loss of NELF-C protein globally redistributes termination factors and perturbs Pol II transcription termination. These changes drive pervasive Pol II transcription into DNA replication zones, leading to transcription-replication conflict that may block the cell cycle in G1 or early S phase. Our findings reveal a previously unrecognized role of NELF in transcription termination and highlight NELF as a potential therapeutic target in colorectal cancer. - Source: PubMed
Publication date: 2026/02/20
Nakayama ChihiroFang QiDaigaku YasukazuAoi YukiIto ShokoTakahashi MamiShimatani ReoMinamisawa TamikoOzturk YagizKimura HiroshiShilatifard AliTellier MichaelNojima Takayuki