HSH2D (aa325_339)
- Known as:
- HSH2D (aa325_339)
- Catalog number:
- Y214480
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- HSH2D (aa325_339)
Related genes to: HSH2D (aa325_339)
- Gene:
- HSH2D NIH gene
- Name:
- hematopoietic SH2 domain containing
- Previous symbol:
- -
- Synonyms:
- ALX, HSH2, FLJ14886
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-31
- Date modifiied:
- 2016-10-11
Related products to: HSH2D (aa325_339)
1-2ml Cryovial Storage Box, As1-2ml Cryovial Storage Box, As Polycarbonate, 100 Place1-2ml Cryovial Storage Box, As Polycarbonate, 100 Place1-2ml Cryovial Storage Box, As Polycarbonate, 100 Place100_Place Cryogenic Box w_Li Holds 1.2 _ 2ml Tubes339
4_(Trifluoromethyl)benzohydrazide alpha,alpha,alpha_Triflu4_Amino_N_(3_trifluoromethyl_phenyl)_be 4_Amino_N_(3_trifluorom5430R Centrifuge, Knob w/ 16 x 5ml AT Rotor6_Fluoroindole 6_Fluoroindoleall-trans-Retinoic Acid Methyl Ester C21H30O2 CAS: 339-16-2all-trans-Retinoic Acid Methyl Ester CAS: 339-16-2 Formula: C21H30O2AMMONIUM FERROUS SULPHATE, (Mohra’s Salt), EXTRA PURE, (NH4)2 Fe(SO4)2.6H2O, CAS 7783_85_9AMMONIUM FERROUS SULPHATE, (Mohra’s Salt), EXTRA PURE, (NH4)2 Fe(SO4)2.6H2O, CAS 7783_85_9anti-CTSB / Cathepsin B (aa42-339) Related articles to: HSH2D (aa325_339)
- T-cell acute lymphoblastic leukemia (T-ALL) originates from the malignant transformation of immature lymphoblasts committed to the T-cell lineage. Relapsed or refractory T-ALL patients show a dismal outcome with limited therapeutic options and cure rates below 10%. Accurate risk stratification is essential for optimizing first-line treatments and maximizing initial complete response rates. Minimal residual disease (MRD) assessment is the most relevant clinical parameter in T-ALL and a direct measure of treatment response, but it requires an initial treatment course that reduces the time for decision-making. Consequently, there is an urgent need to identify novel biomarkers that can predict the response to first-line treatments at diagnosis. By integrating clinical and transcriptomic data from diagnostic T-ALL samples, we found that high MRD patients show a specific transcriptional profile. Moreover, we identified a transcriptional signature characterized by the differential expression of HSH2D, LAT2, BCL2, MAST4, METRN, and PITPNM2 genes that is tightly associated with an increased MRD, which could improve the prediction of poor treatment response in T-ALL patients, especially during early treatment phases. - Source: PubMed
Publication date: 2026/04/09
Lahera AntonioVela-Martín LauraFernández-Navarro PabloLópez-Lorenzo José LuisCornago JavierLlamas PilarPérez-Gómez EduardoMarín-Rubio José LuisFresno ManuelSantos JavierFernández-Piqueras JoséVilla-Morales María - Chronic peritoneal dialysis (PD) induces peritoneal fibrosis through bioincompatible fluid exposure and inflammation. This study aimed to identify fibrosis biomarkers via bioinformatics, assess immune cell correlations, and validate diagnostic utility in clinical/animal models. - Source: PubMed
Publication date: 2025/10/01
Ma XinHe XiaonaWang YunGrzegorzek MarcinLong WenjieChen HongxiGao FangMao NanHuang Xinyu - Chemotherapy, although effective in treating cancer, can induce various cellular responses, including senescence and drug resistance. Here, we investigate the transcriptomic alterations induced by doxorubicin (DOX), a commonly used chemotherapeutic agent, in human colon cancer cells. Using single-cell RNA sequencing, we identified distinct cell populations and their transcriptional profiles following subtoxic DOX treatment, revealing cell clusters characterized by differential expression of genes involved in cell cycle regulation and interferon (IFN) signaling. DOX-persisting proliferating cells exhibited upregulation of genes reported to be linked to the unphosphorylated form of ISGF3 (U-ISGF3) transcription factor. Furthermore, we found that HSH2D, a poor prognostic marker, was highly upregulated in doxorubicin-surviving proliferative cells, and its expression was correlated with U-ISGF3-related genes. Analysis of transcription kinetics via mathematical modeling revealed that the number of mRNA molecules produced per transcriptional burst was increased for U-ISGF3-related genes. We also observed altered gene co-expression patterns of U-ISGF3-related genes and others upon DOX treatment, which potentially contributes to chemoresistance of DOX-surviving proliferative cells and may influence cancer cell fate after chemotherapy. Our findings highlight U-ISGF3-related genes and the JAK/STAT pathway as potential therapeutic targets for overcoming chemoresistance in colon cancer. - Source: PubMed
Publication date: 2024/10/13
Trzaskoma PawelJung SeolKyoungKanno YukaO'Shea John JChow Carson C - P38α is a mitogen-activated protein kinase (MAPK) that mediates inflammatory responses. P38α alterations have been associated with the inflammation-related diseases. However, the role of macrophages-derived p38α in dextran sulfate sodium (DSS)-induced murine experimental colitis remains unclear. - Source: PubMed
Publication date: 2022/04/09
Chen WeiLiang RuiYi YoucaiZhu JinshuiZhang Jing - Specialised pro-resolving mediator (SPM) can dampen the acute inflammation through ERV1, ALX/FPR2 and BLT1 cell receptors and it is conceivable that their expression is dysregulated during chronic inflammation. The aim of this study was to evaluate the expression of ERV1, ALX/FPR2 and BLT1 on peripheral blood (PB) cells from rheumatoid arthritis (RA) patients. - Source: PubMed
Publication date: 2021/09/07
Perniola SimoneBizzoca RitaFornaro MarcoAlivernini StefanoGremese ElisaIannone Florenzo