NELFA Antibody
- Known as:
- NELFA Antibody
- Catalog number:
- XW-7655
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- NELFA Antibody
Related genes to: NELFA Antibody
- Gene:
- NELFA NIH gene
- Name:
- negative elongation factor complex member A
- Previous symbol:
- WHSC2
- Synonyms:
- NELF-A
- Chromosome:
- 4p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-24
- Date modifiied:
- 2015-08-25
Related products to: NELFA Antibody
Related articles to: NELFA Antibody
- The Hippo pathway effector YAP signaling is frequently dysregulated in cancer, promoting transcriptional programs linked to tumor progression. However, how general transcriptional control mechanisms intersect with YAP activity remains unclear. - Source: PubMed
Publication date: 2026/04/22
Vasave Bhavesh SAtreya Aadya AKulkarni Rishabh DNagarkar Sanket SSalvi Khushi RKoppiker C BShashidhara L SKulkarni Madhura D - A minority of 8C-like cells (8CLCs) expressing zygotic genome activation genes are captured in naïve embryonic stem cells (ESCs). However, how human ESCs transition into 8CLCs remains unknown. Here, we show that NELFA is dispensable in human primed ESCs but critical for naïve pluripotency, and its overexpression promotes the primed-to-naïve conversion. Notably, NELFA robustly induces 8CLCs that express human ZGA-specific genes in naïve ESCs. NELFA-induced human 8CLCs can contribute to both embryonic and extraembryonic developmental potential in the interspecies human-mouse chimera assay. Importantly, we also discovered that TP53 can activate the human 8CLCs state, and NELFA might be an upstream regulator of TP53. Furthermore, TP53 and NELFA are both essential for the complete transition to the 8CLC state. We also demonstrate that sustained NELFA overexpression in primed ESCs directs neural lineage specification. Thus, NELFA establishes and maintains naïve pluripotency and drives the 8CLC state, providing insights into early human embryogenesis. - Source: PubMed
Publication date: 2026/05/02
Su XiaominYang FangNeupane JiteshLu ZhiminWu HanGu MeiZhang YongBao SiqinLi XiheSurani M AzimWu Baojiang - 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 - 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 - This study aims to comprehensively characterize the DNA methylation profile in the sperm of patients with Kallmann syndrome (KS), providing new insights into the potential epigenetic mechanisms contributing to the pathogenesis of the disease. - Source: PubMed
Publication date: 2025/10/18
Wang RongrongLi XiaogangZhang JingdiWang XiMao JiangfengFeng XinxinWang SiyuLi YongzheWu XueyanGuo Ye