Ask about this productRelated genes to: HEXIM1 antibody
- Gene:
- HEXIM1 NIH gene
- Name:
- HEXIM P-TEFb complex subunit 1
- Previous symbol:
- -
- Synonyms:
- CLP-1, HIS1, MAQ1, EDG1
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-27
- Date modifiied:
- 2018-11-15
Related products to: HEXIM1 antibody
Related articles to: HEXIM1 antibody
- Frailty, a clinical state of increased vulnerability to stressors with aging, imposes significant strain on healthcare systems. Its genetic underpinnings remain incompletely explored, highlighting the need to identify novel therapeutic targets for aging. - Source: PubMed
Publication date: 2026/04/01
Zhong JiaYuYuan MingHaoZhou EnHu Shuo - Enhanced P-TEFb activity is thought to promote cell proliferation by increasing the transcriptional output of RNA polymerase II. The 7SK snRNP complex, which contains LARP7 and HEXIM1, sequesters and inhibits most cellular P-TEFb to prevent premature transcription elongation. Paradoxically, instead of exerting overgrowth effects, biallelic inactivation of LARP7 is linked to Alazami syndrome, a human neurodevelopmental disorder characterized by growth restriction and cognitive impairment. Here, we report that conditional ablation of either Larp7 or Hexim1 in the murine brain reduces the size and impairs the function of the hippocampal dentate gyrus during the neonatal period. Functional analyses reveal that increased P-TEFb activity enhances self-renewal transcriptional programs in transit-amplifying neuronal progenitor cells to limit neurogenesis in developing dentate gyri. These results demonstrate that dysregulated subtissular stem cell dynamics can reconcile increased P-TEFb activity with reduced organ growth, and suggest a translational opportunity for repurposing P-TEFb inhibitors to treat medical conditions affecting dentate gyrus size and function. - Source: PubMed
Publication date: 2026/03/23
Fang YinQiu TongWang PingBai ShujunWang MinYang ChaoWang YanZhang PeixuanWang HeLiu ShanlingXiao XueLi Qintong - Cognitive processes require de novo gene transcription in neurons. Memory requires the rapid and robust transcription of a class of genes called immediate early genes (IEGs). IEG transcription is facilitated by the formation of a poised basal state, in which RNA polymerase II (RNAP2) initiates transcription, but remains paused downstream of the promoter. Upon neuronal depolarization, the paused RNAP2 is released to complete the synthesis of mRNA transcripts, a process stimulated by positive transcription elongation factor b (P-TEFb). In many cell types, P-TEFb is sequestered into a large inactive complex containing Hexamethylene bisacetamide inducible 1 (HEXIM1), but the impact of this interaction on neuronal gene transcription is not yet fully understood. In this study, we found that neuronal expression levels of HEXIM1 mRNA are highly correlated with impaired cognition in Alzheimer's disease. It is also induced in the hippocampus during memory formation, and following depolarization in neurons. The role of HEXIM1 in neuronal gene transcription was then explored in murine neuronal cultures where we found that calcium frees P-TEFb from the HEXIM1 inhibitory complex. Modulation of P-TEFb by inhibiting the activity of the CDK9 subunit of this complex significantly impacts IEG induction, particularly during repeated depolarization. Our findings indicate that HEXIM1 in complex with P-TEFb plays an important role in establishing and resetting the poised RNAP2 state, enabling efficient activation of genes necessary for synaptic plasticity. - Source: PubMed
Publication date: 2026/02/25
Htet MyoEstay-Olmos CamilaHu LanWu YiyangPowers Brian ECampbell Clorissa DRameshwar AishwaryaAhmed Mohamed RHohman Timothy JWang YanlingSchneider Julie ABennett David AMenon VilasDe Jager Philip LKaas Garrett AColbran Roger JGreer Celeste B - Colorectal cancer (CRC) is a malignant disease that poses a significant threat to human health; however, early diagnostic and treatment strategies for it remain limited. Immune evasion is a critical factor contributing to treatment failure in CRC. Various cell subtypes within the tumor microenvironment (TME) play essential roles in this process. However, there is currently a lack of a systematic and novel classification of immune evasion-related cell subtypes and an analysis of their dynamic interaction networks within the CRC TME. This study aims to explore a novel classification of immune evasion-related subtypes in CRC, elucidate their underlying mechanisms, and assess their value for immunotherapy and prognosis. - Source: PubMed
Publication date: 2026/01/21
Gan QixinXu XuanLiu HaifenLi Yuejun - Hexim proteins are key RNA-dependent regulators of eukaryotic transcription through 7SK-dependent sequestration and inactivation of the kinase P-TEFb (Cdk9-CyclinT1/2) in the 7SK RNP. P-TEFb activity drives release of RNA polymerase II from promoter-proximal pausing for eukaryotic and HIV-1 transcription. The molecular mechanism by which 7SK binding overcomes an intrinsic Hexim autoinhibition for subsequent P-TEFb inactivation has remained unresolved. Here, using NMR and biophysical methods we demonstrate that Hexim1 homodimer engages two high-affinity sites on 7SK RNA. This dual-site binding triggers a conformational rearrangement in Hexim1's disordered central region that unmasks the Cdk9-binding site, which is otherwise sequestered within an inter-monomer dimer interface. These findings reveal how Hexim autoinhibition dictates its specificity for 7SK RNA and prevents premature P-TEFb inhibition in the absence of 7SK, thereby providing a mechanistic understanding of Hexim/P-TEFb assembly into the 7SK RNP and further considerations for understanding Hexim-Tat competition during viral transcription. - Source: PubMed
Publication date: 2026/01/15
Yang YuanMurrali Maria GraziaGalvan SabrinaWang YaqiangStephen ChristineAjjampore NehaWang XiaoyuFeigon Juli