Ask about this productRelated genes to: GBX1 Blocking Peptide
- Gene:
- GBX1 NIH gene
- Name:
- gastrulation brain homeobox 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-30
- Date modifiied:
- 2015-08-27
Related products to: GBX1 Blocking Peptide
Related articles to: GBX1 Blocking Peptide
- The early detection and diagnosis of head and neck squamous cell carcinoma (HNSCC) pose significant challenges. - Source: PubMed
Publication date: 2026/04/24
Xia YichaoLou HuiquanShao ShengjieLiu XiangLi Yongsheng - Acute stress is a powerful inducer of endogenous analgesia. Several brainstem and midbrain areas have been identified that are activated during stress and send descending axons to suppress spinal nociception. The spinal effector circuits and neurons have, however, remained largely elusive. Here, we demonstrate that GABAergic interneurons of the superficial dorsal horn expressing the transcription factor gastrulation brain homeobox 1 (Gbx1) are key elements of these circuits. Their inhibition had little effect on nociception under resting conditions but completely abolished swim stress-induced analgesia. Retrograde monosynaptic tracing revealed input from several brain areas, most prominently from the rostral ventromedial medulla (RVM). Optogenetic circuit tracing demonstrated that this input is inhibitory and that Gbx1 neurons in turn inhibit projection neurons targeting the lateral parabrachial nucleus, a key area in supraspinal pain relay. Our results thus identify a subpopulation of GABAergic neurons in the superficial dorsal horn as key elements of a disinhibitory circuit for stress-induced analgesia. - Source: PubMed
Publication date: 2026/03/16
Haenraets KarenGanley Robert PPietrafesa FrancescaMacDonald Donald IainSousa MaríliaSchalbetter SinaMendes RaquelLuzi FabienneWildner HendrikZeilhofer Hanns Ulrich - Long dismissed as mere genomic parasites, transposable elements (TEs) are now recognized as major drivers of genome evolution. TEs serve as a source of cell-type specific cis-regulatory elements, influencing gene expression and observable phenotypes. However, the precise TE regulatory roles in different contexts remain largely unexplored and the impact of TEs on transcriptional regulatory networks and contribution to disease risk is likely deeply underestimated. - Source: PubMed
Publication date: 2026/01/31
Almeida da Paz MichelleYildiz UmutKim MinyoungCampos-Fornés VíctorPinkasz MarinaDahlet ThomasNoh Kyung-MinTaher Leila - The gastrulation brain homeobox (Gbx) family, including GBX1 and GBX2, is crucial for hindbrain development and contributes to the morphogenesis of the midbrain-hindbrain boundary (MHB). While the role of the GBX1 gene in the development of the human nervous system remains to be elucidated, its variant in humans has not previously been reported to be associated with disease. - Source: PubMed
Zhang BingbingLi XiaohuaQian XiaoTang Jihong - Congenital heart defects (CHDs) are frequently observed in the most common form of Cornelia de Lange Syndrome (CdLS), which is caused by haploinsufficiency for , a gene involved in chromatin looping and cis-regulatory control of gene expression. Here, we surveyed cardiac defects in mice made -haploinsufficient in the second heart field using two Cre drivers: and . Only -driven -haploinsufficiency resulted in CHDs - a finding we traced to the additional contribution of -haploinsufficiency caused by the allele. To test whether combined reduction of and cause CHDs, we made mice globally haploinsufficient for both genes. Indeed, mice exhibited a substantially higher frequency and severity of CHDs than mice haploinsufficient for either gene alone. As a member of the LIM-homeodomain transcription factor family, is involved in chromatin looping and enhancer-promoter communication via a mechanism distinct from that of . Nevertheless, when we performed RNA sequencing on E10.5 hearts from wildtype, , , and embryos, we observed that combined haploinsufficiency resulted in largely additive gene expression changes, including dysregulation of known cardiac regulators ( ) and novel candidates ( ). A subset of additive changes arose from regulatory influences in single mutants that restored gene expression to WT levels in hearts. For example, itself, and (a known target of ), were upregulated in hearts, downregulated in hearts, but expressed at WT levels in hearts. Since loss of upregulation from to hearts coincided with a marked increase in CHDs, we propose that upregulation compensates for the loss of cis- regulatory interactions due to -haploinsufficiency, and protects hearts from severe CHD risk. Supporting this model, other LIM-homeodomain transcription factors ( ) were also upregulated in hearts, with and showing even greater upregulation in hearts. Despite this, CHDs resulting from the combined loss of and were particularly severe. These findings suggest that heart development is exquisitely sensitive to small changes in gene expression, leading to synergistic phenotypic interactions when relatively modest gene expression changes are combined. - Source: PubMed
Publication date: 2025/05/19
Chea StephensonSantos RosayselaLopez-Burks Martha ELander Arthur DCalof Anne L