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
- 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 - Promoter-proximal pausing by negative elongation factor (NELF) establishes a critical checkpoint for RNA polymerase II (RNA Pol II) transcription. Heat shock (HS) induces NELF to form nuclear condensates, yet how their dynamics are regulated and coupled to transcriptional adaptation remains unclear. Using a nanobody-based proximity labeling strategy (NbPro), we identify the molecular chaperones HSPA1A and DNAJB1 as key regulators of NELF condensate dynamics. Although dispensable for initial HS-induced transcriptional repression, chaperone-mediated regulation is required for efficient transcriptional reactivation during recovery. Mechanistically, DNAJB1 recognizes NELFA's tentacle domain and facilitates HSPA1A recruitment, thereby preventing aberrant aggregation and enabling timely condensate disassembly. Disruption of NELF condensate dynamics leads to persistent NELFA phosphorylation, impaired chromatin association, destabilized RNA Pol II pausing, and premature release of non-productive RNA Pol II complexes. Together, these findings reveal a chaperone-dependent mechanism that governs NELF condensate dynamics and highlight promoter-proximal pausing as a checkpoint to prevent immature RNA Pol II escape, rather than merely a means of transcriptional repression. - Source: PubMed
Publication date: 2026/02/06
Jiang ShuyaoJia ZixuanZhu WenxuanLiu YuFu HuanyiZhu FeifengLi ZhuoYang JiayeZhu YiyingSun ZhongxingZhu TianyiQuan XueboJiao HuipengHuang KaiWu ZhibingZou WeiYang BingLu YiZhang LongZhou FangfangFang DongLu Huasong - We previously established distinct roles for the transcriptional elongation factors PAF1, negative elongation factor (NELF), SPT4/5, and SPT6 using auxin-inducible degron systems in human cell lines. Here, we integrate long- and short-read RNA-seq data from these degron lines to quantify transcript isoform usage at single-molecule resolution, identifying elongation factor-specific RNA processing regulons, including a cellular senescence-enriched regulon impacted by NELF and SPT6. Long-term NELF or SPT6 depletion causes reversible growth arrest following early upregulation of senescence-associated genes. Our genetic suppressor screens implicate the elongation factor Elongin A (ELOA) in these effects. ELOA knockout suppresses the progression of RNA polymerase II (RNAPII) past transcription end sites (TESs) at NELF depletion-induced genes. Acute depletion of TES-proximal ELOA causes a loss of RNAPII processivity at the 3' end of genes. ELOA loss also confers a growth advantage to aging primary human fibroblasts. These findings establish NELF/ELOA-dependent mechanisms regulating transcriptional elongation and RNA processing and link them to senescence and aging. - Source: PubMed
Parast SaeidWang SimaiIwanaszko MartaHe YueOlgun Deniz GGold SarahZeidner Jacob MAoi YukiHoward Benjamin CThakur William RRamani VijayShilatifard Ali - Promoter-proximal pausing of RNA polymerase (Pol) II is a key regulatory step during transcription. Despite the central role of pausing in gene regulation, we do not understand the evolutionary processes that led to the emergence of Pol II pausing or its transition to a rate-limiting step actively controlled by transcription factors. Here, we analyzed transcription in species across the tree of life. Unicellular eukaryotes display an accumulation of Pol II near transcription start sites, which we propose transitioned to the longer-lived, focused pause observed in metazoans. This transition coincided with the evolution of new subunits in the negative elongation factor (NELF) and 7SK complexes. Depletion of NELF in mammals shifted the promoter-proximal buildup of Pol II from the pause site into the early gene body and compromised transcriptional activation for a set of heat-shock genes. Our work details the evolutionary history of Pol II pausing and sheds light on how new transcriptional regulatory mechanisms evolve. - Source: PubMed
Publication date: 2025/12/15
Chivu Alexandra GBasso Brent AAbuhashem AbderhmanLeger Michelle MBarshad GiladRice Edward JVill Albert CWong WilfredChou Shao-PeiChovatiya GopalBrady RebeccaSmith Jeramiah JWikramanayake Athula HArenas-Mena CésarBrito Ilana LRuiz-Trillo IñakiHadjantonakis Anna-KaterinaLis John TLewis James JDanko Charles G - Cardiac malformations and ventricular remodeling due to heart diseases result in compromised cardiac function, eventually leading to heart failure. In this study, we examine the role of cardiac Wolf-Hirschhorn Syndrome candidate 2 (Whsc2), Negative elongation factor A (NELFA), one of the genes encoded in the WHS critical region. The Wolf-Hirschhorn Syndrome is a contiguous genetic disorder due to microdeletions in the critical region, with clinical manifestations of neurological defects frequently associated with congenital malformations, including cardiac defects. NelfA has been implicated in RNA polymerase II (pol II) pausing, suggesting a role in pol II-dependent gene transcription. We previously reported an early onset of heart failure with the acute knockdown of NelfA in hearts undergoing pressure overload-induced cardiac hypertrophy. Here, we characterize a mouse model with cardiomyocyte-specific loss of NelfA function, in which these mice develop spontaneous cardiomyopathy at 2 months of age and exhibit early mortality by 3 months, suggesting a critical role for postnatal NelfA in the heart. Interactome data show that chromatin-bound NelfA interacts with proteins involved in chromatin remodeling (Trim28) and pre-mRNA processing (Adrph1l), along with expected binding partners like RNA pol II, Supt5, and other Nelf proteins. Examination of genomic occupancy of these NelfA-associated proteins in the NelfA knockout (KO) hearts reveals a disassembly of the NelfA nucleated complex at promoters of cardiac-enriched genes, including cytoskeletal and metabolic genes. This deconstruction of the NelfA-dependent complex results in the inhibited expression of these essential genes during postnatal cardiac development, leading to a cardiac contractile and metabolic crisis that precipitates dilated cardiomyopathy. - Source: PubMed
Publication date: 2025/10/24
Alikunju SaleenaThakkar ChandniVenkatasubramanian AishwaryaYang ZhiIvessa AndreasSayed Danish