TBX3 antibody - middle region (ARP33412_T100)
- Known as:
- TBX3 (anti-) - middle region (ARP33412_T100)
- Catalog number:
- arp33412_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TBX3 antibody - middle region (ARP33412_T100)
Related genes to: TBX3 antibody - middle region (ARP33412_T100)
- Gene:
- TBX3 NIH gene
- Name:
- T-box 3
- Previous symbol:
- UMS
- Synonyms:
- TBX3-ISO, XHL
- Chromosome:
- 12q24.21
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-18
- Date modifiied:
- 2013-09-05
Related products to: TBX3 antibody - middle region (ARP33412_T100)
Related articles to: TBX3 antibody - middle region (ARP33412_T100)
- Growth hormone (GH) stimulation tests have limited reliability and may lead to false-positive results. - Source: PubMed
Publication date: 2026/05/07
Plachy LukasDusatkova PetraKavciak LukasAmaratunga Shenali AnneSlavenko MatveiDrabova JanaMaratova KlaraNeuman VitObermannova BarboraKolouskova StanislavaSnajderova MartaSumnik ZdenekLebl JanPruhova Stepanka - Oligometastatic disease (OMD) is an intermediate state of metastatic disease in which metastasis-directed therapy (MDT) may improve outcomes. The classification of OMD is inconsistent, typically defined by number of metastases without considering tumor biologic characteristics. To help optimize patient selection for MDT, we analyzed integrated genomic sequencing results from patients with metastatic non-small cell lung cancer (NSCLC). - Source: PubMed
Publication date: 2026/05/14
Wijetunga N AriMankuzhy Nikhil PLebow Emily SBoe Lillian APike Luke R GSchoenfeld Adam JShaverdian NarekChaunzwa Tafadzwa LJones David RChaft Jamie ERudin Charles MKris Mark GYu Helena AChang Jason CIyengar PuneethGomez Daniel R - Histologically normal mammary tissue from breast cancer patients can harbor significant genetic alterations that could precede visible tumor development and influence disease progression. - Source: PubMed
Publication date: 2026/04/30
Andreou MariaChojnowska KatarzynaFilipowicz NataliaHorbacz MonikaMadanecki PiotrDuzowska KatarzynaŁawrynowicz UrszulaDavies HannaBruhn-Olszewska BożenaKoszyński MikołajDrężek-Chyła KingaJaśkiewicz MaciejJąkalski MarcinKostecka AnnaDrzewiecka-Kłysz MartaNowikiewicz MagdalenaLas-Jankowska ManuelaBała DariuszHoffman JacekŚrutek EwaJankowski MichałJankau JerzyHodorowicz-Zaniewska DianaSzpor JoannaSzylberg ŁukaszZegarski WojciechNowikiewicz TomaszBuckley Patrick GTiemann-Boege IreneMieczkowski JakubKoczkowska MagdalenaDumanski Jan PPiotrowski Arkadiusz - Maternal nutrition during critical windows of development plays a pivotal role in shaping long-term disease susceptibility, including cancer risk. This study investigated whether maternal exposure to lipotropes (methyl donor nutrients) during pregnancy and lactation modulates gene expression in 7,12-dimethylbenzanthracene (DMBA)-induced mammary tumors in adult female offspring. Timed-pregnant Sprague-Dawley rats were fed with either a control or lipotrope-supplemented diet, with or without vitamin B6. Female offspring were exposed to DMBA at puberty, and mammary tumors were evaluated histologically and molecularly. DMBA-induced tumors displayed ductal carcinoma in situ-like morphology and significant upregulation of fetal mammary developmental genes ( and ), the tumorigenesis-associated gene , and key epigenetic regulators (, , and ). Estrogen receptor 1 () mRNA expression also showed a significant increase. Maternal lipotropes supplementation significantly attenuated the expression of these genes in offspring tumors. Collectively, these findings demonstrate that maternal methyl donor nutrition modulates tumor-associated gene expression patterns, potentially by limiting the reactivation of developmental and epigenetic pathways in adulthood. This study highlights maternal nutrition as a modifiable early-life factor with important implications for long-term health programming. - Source: PubMed
Publication date: 2026/04/19
Mabasa LawrenceKotze AnriJohnson RabiaRamharack PritikaOmoruyi Sylvester IGabuza Kwazikwakhe BSharma JyotiWillmer Tarryn - The developing vertebrate forelimb expresses seven T-box transcription factors, with several in overlapping expression domains. All T-box transcription family members share similarity within their DNA binding domain, the T-domain. Outside of the T-domain, these factors share little similarity, allowing family members to have different transcriptional properties and binding partners. Several human T-box genes show haploinsufficiency in the limb, including Tbx5 and Tbx3 that, when mutated, cause Holt-Oram and ulnar-mammary syndrome, respectively. This dosage sensitivity combined with the shared T-domain leads to our hypothesis that when co-expressed a competition between T-box factors at target genes can occur. To test this, we ectopically expressed two exogenous T-box factors, T and Tbx6, in the developing forelimb mesenchyme to examine how artificially changing the relative levels of T-box proteins affects forelimb formation. Skeletal, apoptotic, and gene expression assays were used to characterize the resulting phenotypes. While ectopic T and Tbx6 both affected the size and shape of the forearm bones and ossification, they differentially affected digit formation: T caused loss of digits and Tbx6 led to phalange bone duplications and extra digit formation. These dissimilar phenotypes suggest that these transcriptional activators differentially affect pathways critical for regulating forelimb development. - Source: PubMed
Denhart Mariah HChapman Deborah L