GLIS2 antibody - N-terminal region (ARP30037_P050)
- Known as:
- GLIS2 (anti-) - N-terminal region (ARP30037_P050)
- Catalog number:
- arp30037_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GLIS2 antibody - N-terminal region (ARP30037_P050)
Related genes to: GLIS2 antibody - N-terminal region (ARP30037_P050)
- Gene:
- GLIS2 NIH gene
- Name:
- GLIS family zinc finger 2
- Previous symbol:
- -
- Synonyms:
- NPHP7
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-16
- Date modifiied:
- 2014-11-19
Related products to: GLIS2 antibody - N-terminal region (ARP30037_P050)
Related articles to: GLIS2 antibody - N-terminal region (ARP30037_P050)
- This study retrospectively analyzed the clinical manifestations, genetic characteristics, treatment courses, and prognoses of patients with pediatric acute megakaryoblastic leukemia (AMKL) with CBFA2T3::GLIS2 fusion treated at the Institute of Hematology, Chinese Academy of Medical Sciences. Further, the diagnostic and therapeutic features of this rare AMKL subtype, in conjunction with domestic and international literature, were summarized. The patients comprised one male and two females, with a median age at onset of 16 months (range, 8-19 months). Central nervous system leukemia was present at diagnosis in two cases. All were classified as acute myeloid leukemia (AML) -M(7) according to the French-American-British classification, with immunophenotypes demonstrating CD56 positivity and human leukocyte antigen-DR negativity. All patients showed complex abnormal karyotypes, including trisomy 21 in two cases. All patients achieved morphological complete remission (CR) after chemotherapy. However, all patients experienced early relapse, with a median relapse time of 11 months (range, 7-13 months), and the median overall survival time was 16 months (range, 15-47 months). One patient relapsed after the first hematopoietic stem cell transplantation and relapsed again after a second transplantation and is currently receiving palliative care. The other two patients discontinued treatment after relapse and subsequently died. These results reveal that CBFA2T3::GLIS2 fusion-positive AMKL is a highly aggressive subtype, frequently associated with a CD56-positive, HLA-DR-negative immunophenotype, and complex karyotypes, with trisomy 21 observed in a subset of cases. This subtype is characterized by a high relapse rate and an extremely poor prognosis. At present, effective therapeutic approaches are lacking, with an urgent need to explore novel treatment strategies to improve clinical outcomes. - Source: PubMed
Lin SGuo YZhang LChen Y MXiao J GCai X JYang W YChen X J - Advancements in genomic profiling have significantly improved the classification and treatment strategies for acute myeloid leukemia (AML). However, widely utilized molecular diagnostic techniques, including targeted gene panels, are often insufficient for detecting complex structural variants, cryptic fusions, and poorly characterized driver mutations. Here, we present the case of a 15-month-old female with pediatric acute megakaryoblastic leukemia (AMKL) who exhibited an atypical clinical presentation. Initial imaging revealed expansile lesions in the pelvic bones and vertebral bodies, prompting suspicion of malignancy. Conventional diagnostics, including immunohistochemistry and targeted sequencing, failed to identify a definitive oncogenic driver. Whole genome sequencing (WGS) identified a fusion, leading to a revised AMKL diagnosis with a RAM immunophenotype. The patient underwent induction chemotherapy with cytarabine and mitoxantrone, followed by salvage therapy with venetoclax and azacitidine, resulting in morphologic remission. Subsequent haploidentical hematopoietic stem cell transplantation achieved remission, with ongoing hematologic recovery. This case underscores the limitations of conventional molecular assays in detecting cryptic fusions and highlights the critical role of comprehensive genomic profiling in refining subclassification and optimizing therapeutic strategies in pediatric AML. - Source: PubMed
Publication date: 2026/03/25
Lee YunaChoi Jung YoonPark Hyun JinKim Bo KyungKim Hyun KyungKim YeseulCheon Jung-EunPark Sung-HyePhi Ji HoonLee Ji WonKim RyulKoh June-YoungKang Hyoung Jin - COVID-19 patients readily present with severe epithelial damage, such as tissue ulceration and erosion, along with disrupted tissue repair, in multiple organs. The mucous membranes of the lung alveoli [1, 2], gastrointestinal tract [3, 4], nasal [5] and oral cavity [6, 7] are the primary targets of the SARS-CoV-2 virus. The infected epithelium triggers a dysregulated immune response that further damages tissues and organs [8-10]. Increasing evidence suggests that the SARS-CoV-2 virus can cause direct damage to epithelial cells and fibroblasts [11-13]. Here, we report that the mucosa epithelia of COVID-19 patients can undergo cellular dedifferentiation before any pathological features are observed. SARS-CoV-2 nonspike structural proteins, particularly the Envelope protein, can rapidly induce epithelial cell dedifferentiation, micronuclei formation, cell cycle arrest at the G1 phase and apoptosis. The protein can also severely affect the progenitor cell stratification program. Mechanistically, we identified a unique molecule, calponin 2 (CNN2), as a downstream effector of nonspike structural proteins. Moreover, CNN2 levels were elevated in the epithelia of COVID-19 patients. Downregulating CNN2 could inhibit epithelial cell apoptosis and promote cell differentiation. CNN2 expression is negatively regulated by GLIS2, a transcription factor associated with the disruption of ciliary dynamics in epithelial cells. Therefore, we propose that SARS-CoV-2 damages mucosal epithelium integrity via a novel "double hijack" mechanism: inducing dedifferentiation and disrupting stratification and suggest a new therapeutic target: CNN2 for COVID-19 treatment. - Source: PubMed
Publication date: 2026/03/23
Gao YanSouza Lucas LacerdaKang Hong SoonLi ZehanHernandez-Guerrero Juan CarlosAlves Fábio AbreuZhang WeiSharma VikramHanks SallyYu JinhuaTredwin ChristopherJetten Anton MSoares Ciro DantasHu Bing - - Source: PubMed
Publication date: 2026/02/12
- RNA sequencing from 262 patients with paediatric acute myeloid leukaemia (AML) (JPLSG AML-12) was deconvoluted employing adult single-cell RNA-sequencing signatures and Zeng's method, which defined five cellular hierarchy subtypes: primitive, leukaemic stem/progenitor cell (LSPC)-Cycle, ProMono-like, granulocyte-monocyte progenitor (GMP)-like and intermediate. Principal component analysis revealed two main axes that distinguish paediatric from adult AML, with notable LSPC-Cycle and ProMono-like phenotype enrichment. LSPC-Cycle (>25% cycling stem-like cells) had proliferative and quiescent LSPCs, frequent French-American-British (FAB)-M7 and worst prognosis (overall survival odds ratio vs. GMP-like: 11.33). Morphology was related to the primitive (FAB-M0), GMP-like (M2/M4) and ProMono-like (M5) groups. Genomic patterns aligned with hierarchy: CBFA2T3::GLIS2, MYB::GATA1 and MECOM high expression in LSPC-Cycle; CBFB::MYH11, NUP98::NSD1 and NPM1 in the intermediate; and DEK::NUP214 and NUP98::KDM5A were concentrated in the primitive group. bZIP CEBPA and FLT3-ITD mutations clustered in the intermediate and primitive groups. Most of RUNX1::RUNX1T1 clustered in the intermediate group, whereas KMT2A::MLLT3 hierarchy differed with MECOM expression level. Paediatric AML comprised more primitive cells, rarely with mono-like/cDC-like dominance. LSPC-Cycle, FLT3-ITD and NUP98::KDM5A were considered independent prognostic factors in multivariate analysis. Findings indicate the prognostic relevance of cellular hierarchy and the importance of integrating hierarchy-specific molecular profiles for improved risk stratification and treatment formulation. - Source: PubMed
Publication date: 2026/02/03
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