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
- Extranodal NK/T-cell lymphoma (ENKTL) of the central nervous system (CNS) is very rare. We herein report a case of ENKTL originating from the CNS in a 79-year-old woman. The patient presented with episodic seizures, left-sided limb weakness, altered mental status, and dysarthria for more than 1 month. Radiological examination revealed a solitary mass in the (laterality) frontal lobe of the brain, which was surgically removed. Histopathology revealed a tumor showing diffuse growth of large anaplastic cells with multiple reniform nuclei, horseshoe nuclei, and doughnut-like nuclei. Immunohistochemically, the tumor cells were diffusely positive for CD3, CD30, Gramazyme B, and TIA1 and negative for ALK and CD56. It was almost misdiagnosed as ALK-negative anaplastic large cell lymphoma, but positivity for cytotoxic markers and EBER-ISH helped establish the diagnosis of ENKTL. To the best of our knowledge, this anaplastic variant of ENKTL has not been reported in the CNS. We present this case to describe an uncommon aggressive variant of ENKTL at CNS as a rare location with diagnostic pitfalls. - Source: PubMed
Publication date: 2026/09/03
Chen HuanShi LiuLi JiaSiZhang Feng - Overactivation of Microtubule affinity regulating kinase 4 (MARK4) is believed to contribute to Alzheimer's disease pathogenesis. MARK4 promotes the accumulation of the microtubule-binding protein tau, thereby enhancing tau-induced neurodegeneration. However, the underlying mechanisms by which MARK4 enhances tau accumulation are not fully understood. T-cell intracellular antigen 1 (TIA1), a critical regulator of stress granule (SG) formation, has been suggested to initiate tau abnormality. Here, we report that MARK4 and TIA1 synergistically induce stress granule (SG) formation. MARK4 is localized in SGs with TIA1 in mammalian cultured cells and primary neurons. MARK4 suppresses TIA1 dimerization and enhances SG formation under oxidative stress. Co-expression of MARK4 and TIA1 promotes tau accumulation, and knockdown of a fly ortholog of TIA1 suppressed tau toxicity in a Drosophila model. These results identify MARK4 as a novel regulator of SG formation and suggest a mechanistic link between oxidative stress and tau pathology. - Source: PubMed
Publication date: 2026/09/04
Nakajima ShoWatanabe KotoneSultanakhmetov GrigoriiFukuchi AoiIto KeiyaShimizu SawakoSaito TaroAsada AkikoAndo Kanae - 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