NELFA Antibody
- Known as:
- NELFA Antibody
- Catalog number:
- XW-7656
- 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
- 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 - SAYP and Bap170, subunits of the SWI/SNF remodeling complex, have the ability to support enhancer-dependent transcription when artificially recruited to the promoter on a transgene. We found that the phenomenon critically depends on two subunits of the Mediator kinase module, Med12 and Med13 but does not require the two other subunits of the module (Cdk8 and CycC) or other subunits of the core part of the complex. A cooperation of the above proteins in active transcription was also observed at endogenous loci, but the contribution of the subunits to the activity of a particular gene differed in different loci. The factors SAYP/Bap170 and Med12/Med13 did not form sufficiently stable interactions in the extract, and their cooperation was apparently local at regulatory elements, the presence of SAYP and Bap170 in a locus being necessary for stable recruitment of Med12 and Med13 to the locus. In addition to the above factors, the Nelf-A protein was found to participate in the process. The cooperation of the factors, independent of enzymatic activities of the complexes they are part of, appears to be a novel mechanism that maintains promoter activity and may be used in many loci of the genome. Extended intrinsically disordered regions of the factors were assumed to sustain the mechanism. - Source: PubMed
Publication date: 2024/11/28
Shidlovskii Yulii VUlianova Yulia AShaposhnikov Alexander VKolesnik Valeria VPravednikova Anna EStepanov Nikita GChetverina DaryaSaccone GiuseppeLebedeva Lyubov AChmykhalo Victor KGiordano Ennio - Chromosome 4p16.3 microdeletions are known to cause Wolf-Hirschhorn syndrome (WHS), which is characterized by a distinct craniofacial gestalt and multiple congenital malformations. The 4p16.3 region encompasses WHS critical region 1 (WHSCR1) and 2 (WHSCR2). The WHSCR contains several genes that have been implicated in the WHS phenotype including: WHS candidate 1 [WHSC1 (aka NSD2, OMIM 602952)], WHS candidate 2 [WHSC2 (aka NELFA, OMIM 606026)], and LETM1 (OMIM 604407). Although several patients harboring 4p16.3 microdeletions that are associated with WHS phenotypes have been reported, the precise molecular underpinnings of WHS are subjects of active investigations. The potential role(s) of genes within the 4p16.3 are increasingly being investigated. Here we report a novel 4p16.3 terminal microdeletion that is not associated with the characteristic WHS phenotype. We studied Individual A (7-months-old female) and her father, Individual B (27-year-old), who both carry a terminal 4p16.3 microdeletion (about 555 kb) that is distal to the WHSCR1 and WHSCR2, and does not include WHSC1, WHSC2, or LETM1. Overall, our findings expand the phenotypic spectrum associated with 4p16.3 microdeletions and support the previous observations that, in some individuals, microdeletions within 4p16.3 region may not be sufficient to cause WHS. - Source: PubMed
Publication date: 2024/11/07
Osundiji Mayowa AzeezKahn EvaLanpher Brendan