TROP2 _ TACSTD2 Antibody
- Known as:
- TROP2 _ TACSTD2 Antibody
- Catalog number:
- 10428-R030
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- TROP2 _ TACSTD2 Antibody
Related genes to: TROP2 _ TACSTD2 Antibody
- Gene:
- TACSTD2 NIH gene
- Name:
- tumor associated calcium signal transducer 2
- Previous symbol:
- M1S1
- Synonyms:
- TROP2, GA733-1, EGP-1
- Chromosome:
- 1p32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-11-20
- Date modifiied:
- 2019-03-01
Related products to: TROP2 _ TACSTD2 Antibody
Related articles to: TROP2 _ TACSTD2 Antibody
- Acquired resistance limits the therapeutic efficacy of KRAS-MAPK inhibitors in pancreatic ductal adenocarcinoma (PDAC). As transcriptional plasticity and epithelial-to-mesenchymal transition (EMT) have been implicated in resistance, we sought to study the molecular mechanisms driving these changes to uncover actionable vulnerabilities. Sustained KRAS-MAPK inhibition induced interferon and NF-κB signaling and promoted cell state change mimicking an EMT state associated with drug resistance. Network analysis identified the interferon-inducible E3 ubiquitin ligase TRIM22 as a central regulator of this response. Mechanistically, TRIM22 promoted proteasomal degradation of IκBα, resulting in sustained NF-κB and EMT program activation that coincided with a basal-like transcriptional cell state. TRIM22 expression was driven by IRF1 and IRF9 following relief of ERK-mediated transcriptional repression during pathway inhibition. EMT induction was accompanied by marked upregulation of TROP2 (TACSTD2), an NF-κB target gene enriched in basal-like PDAC cell states. Combining TROP2-directed antibody-drug conjugate sacituzumab govitecan with KRAS or ERK inhibitors significantly suppressed PDAC tumor growth in xenograft models. Overall, prolonged KRAS-MAPK inhibition activates an interferon-TRIM22-NF-κB axis that drives EMT and therapeutic resistance in PDAC, while revealing TROP2 as a clinically actionable vulnerability to overcome acquired resistance. - Source: PubMed
Publication date: 2026/04/20
Bulle AshenafiChen YaliLi HuapingChen Timothy Hung-PoKhawar Iftikhar AliLi LinWang YuLiu PengSomani Vikas KumarKurupi RichardGeng YutongPereye Ofejiro BlessingBansod SapanaLe Son BRuzinova Marianna BTran David DLim Kian-Huat - Concordance of NECTIN-4 gene and protein expression and clinic-pathologic associations in matched bladder cancer (BC) triplets, defined as histological specimens from transurethral resection of the bladder (TUR-B), radical cystectomy (RC), and lymphadenectomy (LA) from the same patient, remains unknown. With Enfortumab Vedotin (EV) potentially moving into earlier treatment settings, understanding expression of NECTIN-4 and other targets in archival tissue samples is important. This study characterized protein expression of NECTIN-4 and gene expression of NECTIN4, TACSTD2, ERBB2, PD-L1 and PD1 in matched BC triplet specimens and correlated findings with survival endpoints. - Source: PubMed
Publication date: 2026/04/14
Uysal DanielReible BrunoWildner LukasSteidler AnnetteStöth ManuelWessels FrederikNientiedt MalinWorst Thomas StefanErben PhilippEgen LuisaNitschke KatjaBrochhausen ChristophMichel Maurice StephanNuhn PhilippKowalewski Karl-Friedrich - Gelatinous drop-like dystrophy is a rare autosomal recessive disorder caused by pathogenic variants in the gene and characterized by subepithelial amyloid deposits in the cornea. Alterations in are seen in lymphedema-distichiasis syndrome, in which patients classically exhibit lymphedema of the extremities and a double row of eyelashes. This report links alterations in the gene to a corneal phenotype that is histologically identical to that seen in gelatinous drop-like dystrophy. - Source: PubMed
Publication date: 2026/04/11
Sexton GabrielOury Nadine HTripi Kelly SchoopingNischal Ken KChu Charleen T - Androgen deprivation induces extensive tissue remodelling in the prostate, characterized by epithelial cell attrition and acquisition of a progenitor-like state in residual luminal epithelial cells. The mechanisms driving differentiated epithelial cells toward a progenitor fate remain unclear. Here, we identify that prostate regression is mediated by the engulfment of apoptotic neighbours by epithelial cells and that efferocytosis promotes acquisition of a progenitor-like state. We show that epithelial cells are the predominant phagocytes during regression, engaging in temporally coordinated waves of apoptotic cell clearance. This process is accompanied by marked metabolic reprogramming, including increased aerobic glycolysis and lactate production. This coincides with enhanced histone lysine-lactylation at promoters of genes involved in autophagy, apoptosis regulation, and luminal progenitor identity. Blockade of efferocytosis in vivo via epithelial-specific expression of the dominant negative phosphatidylserine binding protein MFGE8-D89E impaired prostate regression and compromised the induction of the luminal progenitor marker Tacstd2. These findings reveal that epithelial efferocytosis is an essential mechanism that couples cell clearance and epithelial plasticity. This work establishes epithelial efferocytosis as a determinant of cell state transitions in the prostate, with implications for a direct role in castration-resistant prostate cancer and other regenerative or remodelling processes. - Source: PubMed
Publication date: 2026/04/10
Graham-Paquin Adda-LeeSaini DeepakViala SophieWhitford Mara KmTremblay MathieuPastor William ABouchard MaximeMcCaffrey Luke - Immune exclusion inhibits antitumor immunity and response to immunotherapy, but its mechanisms remain poorly defined. In triple-negative breast cancer (TNBC), an aggressive and generally immune-rich subtype, an immune-cold microenvironment predicts poor prognosis due to a limited response to chemotherapy and immune checkpoint inhibitors. This study aimed to identify mechanisms regulating immune infiltration in TNBC. - Source: PubMed
Publication date: 2026/04/03
Wu BogangThant WinBitman ElenaLiu TingLiu JiePaschalis Eleftherios IPatel Bidish KNawrocki ColeXu Katherine HNieman Linda TTing David Tde Gois Macedo BrunaCheng YangJiang KevinSun FengfeiThimmiah NayanaSun ShengAbelman Rachel OBossuyt Veerle IIsakoff Steven JSpring Laura MBardia AdityaEllisen Leif W