Ask about this productRelated genes to: TIA1 antibody
- Gene:
- TIA1 NIH gene
- Name:
- TIA1 cytotoxic granule associated RNA binding protein
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-01
- Date modifiied:
- 2016-10-05
Related products to: TIA1 antibody
Related articles to: TIA1 antibody
- Type 1 and type 2 diabetes are characterized by beta cell dysfunction and insulin deficiency, and the appropriate turnover of MYC expression appears to control the beta-cell fate. Therefore, it is important to better understand the mechanism that controls MYC expression. Hence, the current study aimed to elucidate the interactions of the long non-coding RNA molecule PHAROH at the interface of MYC mRNA and the RNA-binding protein TIA1. For this purpose, we studied MYC mRNA levels in glucagon-producing alpha-TC1-6 cells, insulin-producing MIN6 cells, and in human pancreatic islets. We observed that in insulin-producing cells, but not in alpha cells, MYC mRNA levels were increased in response to stress (proinflammatory cytokines or palmitate + high glucose). Levels of PHAROH were also increased in insulin-producing cells, but not in glucagon-producing cells. To evaluate whether the increased PHAROH levels participated in the induction of MYC mRNA, we treated MIN6 cells with synthetic antisense LNA GapmeR oligonucleotides (ASO) designed to target PHAROH. We observed that the PHAROH ASO 1 increased both PHAROH and MYC mRNA expression. MYC protein levels were also increased by PHAROH ASO 1, both in the absence and presence of pro-inflammatory cytokines. Using an RNA immunoprecipitation strategy, we observed that PHAROH ASO 1 decreased MYC mRNA binding to TIA1, and instead increased PHAROH binding to TIA1. It is concluded that beta cells increase their MYC expression during stress and that this occurs via increased PHAROH-mediated sequestration of TIA1 and subsequent release of MYC mRNA from TIA1-induced inhibition. - Source: PubMed
Publication date: 2026/08/18
Zhao TongjianWelsh Nils - Immune checkpoint inhibitors (ICIs) have revolutionized the management of gastric cancer; however, they can lead to rare immune-related adverse events (irAEs) affecting the urinary system. Herein, we report a case of non-bacterial cystitis complicated by acute kidney injury (AKI) in a 59-year-old male patient with Alpha-fetoprotein-producing gastric carcinoma (AFP-GC). Following treatment with toripalimab combined with SOX chemotherapy, the patient developed urinary tract irritation symptoms, gross hematuria, and stage II AKI. Cystoscopy revealed diffuse mucosal hemorrhage, and biopsy demonstrated extensive infiltration of CD3, CD8, CD4, and CD20 lymphocytes, along with high PD-L1 expression and TIA-1 positivity, confirming the diagnosis of non-bacterial cystitis. A full-dose methylprednisolone pulse of 200 mg/day effectively alleviated the symptoms and restored renal function. This case underscores the importance of vigilance for urinary system irAEs in patients receiving ICIs, emphasizing that early identification and systematic evaluation are critical. Full-dose corticosteroids should be used for moderate to severe irAEs. Moreover, this report provides valuable insights into immunotherapy practice and toxicity management in the rare AFP-GC subtype. - Source: PubMed
Publication date: 2026/07/14
Li ZhenpengYi XiuxiuFu JieLiang YanZhang SensenYang XvDu Zhonghai - Myopathies are a heterogeneous group of disorders that primarily affect skeletal muscles and are classified as rare diseases owing to their low incidence. In particular, Welander distal myopathy is a rare, late-onset muscular disorder that was first described in 1951. Since then, substantial progress has been made in characterizing its clinical presentation and histopathological features. Despite these advances, many aspects of the disease, such as the underlying molecular mechanisms and factors driving phenotypic variability, remain unknown. Furthermore, the scarcity of reliable disease models not only limits the exploration of the molecular basis of the disease but also the development of effective treatments. In this review, we summarize the current knowledge of Welander distal myopathy and discuss potential directions in this field. - Source: PubMed
Publication date: 2026/07/21
García-Rubio AnaDe Los Santos Julia SánchezIzquierdo José M - Primary Cutaneous Anaplastic Large Cell Lymphoma (PCALCL) is a CD30-positive T-cell lymphoma that typically manifests as a dermal nodule or tumor with favorable prognosis. Rare morphologic variants with prominent myxoid stroma can closely mimic myxoid soft tissue sarcomas and lead to misdiagnosis. A 40-year-old man presented with a slowly enlarging ulcerated mass on the left thigh that was radiologically regarded as a superficial soft tissue sarcoma, prompting wide excision with sentinel lymph node biopsy. Histological examination showed a multinodular, dermal, and subcutaneous tumor composed of highly pleomorphic hallmark-type, rhabdoid, epithelioid, and spindle cells, along with multinucleated forms embedded in abundant myxoid stroma, and associated with delicate curvilinear vessels. Immunohistochemically, all tumor cells demonstrated strong and diffuse CD30, CD2, and CD4 expression; and weak positivity for EMA. They were negative for CD3, CD5, CD7, CD8, TIA-1, and perforin, and also showed no expression of ALK or of epithelial, melanocytic, myogenic, vascular, or B-cell markers. These findings support the diagnosis of ALK-negative myxoid PCALCL. Comprehensive staging with positron emission tomography-computed tomography and bone marrow biopsy revealed no extracutaneous disease, and the patient achieved a complete metabolic remission after 6 cycles of CHOP-E chemotherapy, remaining disease-free for 40 months after diagnosis. This case broadens the clinicopathologic spectrum of PCALCL and highlights that infiltrative and myxoid CD30-positive tumors of the extremities may masquerade as sarcoma, underscoring the importance of including CD30 and T-cell markers in the evaluation of pleomorphic myxoid soft tissue tumors. - Source: PubMed
Publication date: 2026/07/06
Haiduk Ihar IPodyacheva Oxana AVladimirkina Maria SDavydova Diana AArtemyeva Anna SValkov Andrey Y - Hepatitis C virus (HCV) exploits lipid droplets (LDs) during the production of infectious particles. Although several host factors, including stress granule (SG) proteins, have been reported to localize to LDs in HCV-infected cells, the mechanism by which these proteins are recruited to LDs has remained unclear. In this study, we show that Ras-GAP SH3 domain-binding protein 1 (G3BP1), an essential SG component, is recruited to LDs with a time lag of several hours or more after the HCV Core protein accumulates on LDs following infection, and that G3BP1 retains its ability to assemble SGs even when localized to LDs during the late phase of infection. Treatment of HCV-infected cells with compounds that disrupt liquid-liquid phase separation (LLPS) abolished the LD localization of G3BP1, as well as another SG protein, T-cell intracellular antigen-1, whereas the LD localization of the viral proteins Core and NS5A was not affected. Finally, we demonstrate that ectopic expression of HCV Core alone is insufficient to recruit G3BP1 to LDs; however, co-expression of Core together with subgenomic HCV RNA, even a replication-defective replicon RNA, leads to the accumulation of G3BP1 around LDs. Collectively, these findings suggest that during the HCV life cycle, the initial localization of Core to LDs, followed by the recruitment of newly synthesized viral RNA to the LD surface, drives LLPS-mediated assembly of biomolecular condensates containing G3BP1 and other host SG proteins around LDs.IMPORTANCEDuring the late stages of hepatitis C virus (HCV) infection, various viral and host proteins are known to accumulate around lipid droplets (LDs), where virion assembly is thought to occur. However, it has remained unclear how the expression of a limited subset of viral factors can induce such an extensive cellular reorganization. Here, we identify that HCV infection induces the relocalization of the stress granule (SG)-associated proteins G3BP1 and TIA-1 onto LDs through liquid-liquid phase separation (LLPS). We further demonstrate that the minimal requirement for G3BP1 recruitment to LDs is the coexistence of the HCV Core and the viral RNA. Because G3BP1 plays a central role in the interaction network underlying SG formation and is capable of mobilizing additional SG components, our findings suggest that LLPS-dependent assembly of biomolecular condensates occurs around LDs during HCV infection. This work provides mechanistic insight into HCV particle formation, including viral genome packaging, and offers a conceptual basis for developing future antiviral strategies. - Source: PubMed
Publication date: 2026/06/26
Jiao MengyuKonno AluWang XiaoweiLiu JieIto MasahikoSatoh ShinyaSuzuki RyosukeIwatani YasumasaSuzuki Tetsuro