Ask about this productRelated genes to: CD117 antibody
- Gene:
- KIT NIH gene
- Name:
- KIT proto-oncogene, receptor tyrosine kinase
- Previous symbol:
- PBT
- Synonyms:
- CD117, SCFR, C-Kit
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: CD117 antibody
Related articles to: CD117 antibody
- ObjectiveThe molecular pathogenesis of intracranial aneurysms remains undefined despite its central role in aneurysmal subarachnoid hemorrhage, a major cause of stroke and shock. Although exosomal micro ribonucleic acids have emerged as key regulators in intracranial aneurysm progression, the specific contributions of micro ribonucleic acid-154-5p remain underexplored.MethodsUsing quantitative reverse transcription polymerase chain reaction, we assessed the micro ribonucleic acid-154-5p expression in intracranial aneurysm specimens. Transmission electron microscopy was used to validate the extracted exosome. Exosomal transfer was confirmed using Cy3-labeled micro ribonucleic acid tracing and quantitative reverse transcription polymerase chain reaction. Functional impacts on vascular smooth muscle cells were evaluated using Cell Counting Kit-8, apoptosis, and 5-ethynyl-2'-deoxyuridine assays. Target genes were identified via ribonucleic acid pull-down and luciferase reporter assays.ResultsHerein, micro ribonucleic acid-154-5p levels were upregulated in intracranial aneurysms. Furthermore, micro ribonucleic acid-154-5p promotes the intracranial aneurysm phenotype in vascular smooth muscle cells. HO-exposed vascular smooth muscle cells secrete exosomal micro ribonucleic acid-154-5p, which can be transferred to other vascular smooth muscle cells. Exosomal micro ribonucleic acid-154-5p promotes the development of intracranial aneurysms phenotype in vascular smooth muscle cells by targeting myosin light chain kinase.ConclusionsExosomal micro ribonucleic acid-154-5p is a novel potentially associated and promising therapeutic target for intracranial aneurysm management. However, the current study is limited to in vitro evidence. - Source: PubMed
Publication date: 2026/09/04
Song JinhaiLuan WenkangChu LiangPan PengjieQian YaoLu Yunpeng - This report describes the histopathological and immunohistochemical findings of a noninvasive malignant mammary adenomyoepithelioma in a seven-year-old neutered male mixed-breed cat. The animal was euthanized due to an extensive mandibular fracture caused by squamous cell carcinoma. Macroscopically, a 3 × 1.5 cm, elevated, well-defined, ulcerated, lobulated, reddish-white, solid - occasionally cystic - and firm nodule was observed in the right inguinal mammary gland. Microscopically, an expansive neoplastic proliferation composed of myoepithelial and epithelial cells arranged predominantly in a papillary pattern was observed. Immunohistochemistry was performed for the markers C-Kit, pan-cytokeratin (CK-AE1/AE3), cytokeratin 7 (CK7), P63, estrogen receptor (ER), progesterone receptor (PR), Ki67, cyclooxygenase-2 (Cox-2), and GATA3. The neoplastic cells were positive for CK AE1/AE3 and 7 (epithelial cells), P63 (myoepithelial cells), Cox-2 (epithelial and myoepithelial cells), and PR (epithelial cells). Positive results for CK-AE1/AE3, CK7, and P63 confirmed the epithelial and myoepithelial nature of the tumor, the mitotic index and elevated Ki-67 expression supported the interpretation of a malignant proliferative phenotype and contributed to the classification of the lesion as a noninvasive malignant adenomyoepithelioma. Based on the macroscopic, microscopic, and immunohistochemical findings, a diagnosis of noninvasive malignant mammary adenomyoepithelioma was established. - Source: PubMed
Publication date: 2026/09/04
Pastor Felipe MartinsFerreira EnioTaborda Daiana Yively Osórioda Silva Martinez Nayara ToledoCassali Geovanni DantasSerakides RogériaOcarino Natália Melo - Mucosa‑associated lymphoid tissue lymphoma translocation protein 1 (MALT1) is a key paracaspase enzyme regulating immune responses, inflammation and oxidative stress. The present study aimed to investigate the effect of MALT1 inhibition on neuroinflammation, neuronal loss and oxidative stress in Alzheimer's disease (AD). A co‑culture system involving microglia and neuron cells under β‑amyloid (Aβ) intervention was used to establish AD cellular models using human microglia HMC3 cells and neuroblastoma SH‑SY5Y cells and mouse microglia BV‑2 and hippocampal neuron HT‑22 cells. The inhibition of MALT1 proteolytic activity was achieved by MALT1 inhibitor 2 (MI‑2) treatment, and the NF‑κB pathway was activated by phorbol 12‑myristate 13‑acetate (PMA) treatment in HMC3 and BV‑2 cells. Western blotting, ELISA, Cell Counting Kit‑8, EdU staining, reactive oxygen species (ROS) detection and reduced glutathione (GSH) assays were performed to evaluate molecular changes, inflammatory responses, neuronal viability and oxidative stress. MALT1 expression was upregulated following Aβ treatment in HMC3 and BV‑2 cells. MALT1 inhibition by MI‑2 suppressed the microglial M1 phenotype but enhanced the M2 phenotype, reduced the levels of the proinflammatory cytokines TNF‑α and IL‑1β and inactivated the NF‑κB pathway in HMC3 and BV‑2 cells. Moreover, microglial MALT1 inhibition elevated cell viability (verified by Cell Counting Kit‑8 and EdU assays), increased the level of reduced glutathione and decreased the levels of reactive oxygen species in SH‑SY5Y and HT‑22 cells. NF‑κB activation by PMA attenuated the effects of MALT1 inhibition on the microglial phenotype switch and proinflammatory cytokine secretion in HMC3 and BV‑2 cells, as well as cell viability and oxidative stress in SH‑SY5Y and HT‑22 cells. The present study reveals that MALT1 inhibition may suppress microglial M1 phenotype, neuroinflammation, neuronal loss and oxidative stress by inactivating the NF‑κB pathway in AD. - Source: PubMed
Publication date: 2026/09/04
Li YuanlongFan HuaHan XiongNi MingHou XiaodanXia HailanShi YinzhuZhang LinSun Jun - Major depressive disorder is a disabling psychiatric illness with a growing global burden. Neuroinflammation, particularly microglial polarization, is increasingly recognized as a key pathogenic factor and is closely linked to lipid metabolic regulation. Shikonin, a bioactive naphthoquinone from , exhibits anti-inflammatory and antioxidant properties, yet its antidepressant effects remain unclear. This study examined whether shikonin alleviates depressive-like behaviors by suppressing neuroinflammation. - Source: PubMed
Chai ZiLiu Wen-TingLiu Han-YangSu Yuan-YuanMa Su-YuanLiang Hong-TaoLi Ya-QinLiu Rui - Rare-earth single-atom nanozymes (RESAzymes) have emerged as promising catalysts due to their maximized atom utilization efficiency and tunable enzymatic activities. Herein, a colorimetric-Surface-enhanced Raman scattering (SERS) dual-modal sensing platform is constructed to introduce 4f electron configurations of single-atom ytterbium active site decorated on a nitrogen-doped porous carbon (Yb-N/C) by a facile hierarchical cascade-anchoring protocol. Specifically, this unique coordination environment can promote substrate molecule adsorption and activation energy barriers, possessing excellent peroxidase (POD)-mimicking activity and SERS enhancement performance in TMB-HO system. In the presence of glutathione (GSH), Yb-N/C catalyst is inhibited to result in reducing oxTMB for returning its colorless state, consequently diminishing both the colorimetric readout and the SERS intensity. Interestingly, this reaction mechanism from Yb-N/C is systematically illustrated through the steady-state kinetic, electron paramagnetic resonance (EPR), and density functional theory (DFT) calculations. Notably, the limited of detection (LOD) of GSH with colorimetric and SERS dual-mode was as low as 0.30 and 0.11 µM, respectively. Our established dual-modal analysis for intracellular GSH exhibits the favorable consistent with the standard kit in HepG2, KYSE150, and MCF-7 cells, respectively. This work will offer an in-depth understanding of RESAzymes-mimicking activity of colorimetric-SERS biosensors by adjusting electronic structures in carbon-based carrier. - Source: PubMed
Publication date: 2026/09/04
Zhao HuifangChen YiLiu LiliPeng FujuanGuan BoweiLi JinzeWang QianLiao LuliangChi BaozhuZhang Ruiping