STAM2
- Known as:
- STAM2
- Catalog number:
- Y213526
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- STAM2
Related genes to: STAM2
- Gene:
- STAM2 NIH gene
- Name:
- signal transducing adaptor molecule 2
- Previous symbol:
- -
- Synonyms:
- Hbp
- Chromosome:
- 2q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-14
- Date modifiied:
- 2015-11-19
Related products to: STAM2
Related articles to: STAM2
- Complex fusiform aneurysms of the middle cerebral artery (MCA) bifurcation remain challenging when the diseased segment incorporates both M2 trunks, precluding reconstructive clipping or endovascular options. We present a video article demonstrating a tailored dual revascularization strategy for a fusiform MCA bifurcation aneurysm involving both M2 divisions. Through a frontotemporal approach with wide sylvian fissure dissection, the aneurysm and the origins of the superior and inferior M2 trunks were exposed. Donor selection and bypass configuration were guided by the anticipated flow requirements of each M2 division, estimated from recipient territory, relative vessel caliber, and intraoperative Doppler assessment: an internal maxillary artery-radial artery (IMax-RA) graft was used to revascularize the larger-caliber M2 trunk supplying the larger territory and judged to require higher flow, while a superficial temporal artery (STA)-M2 bypass was performed for the second M2 division with lower anticipated flow demand. Only one suitable STA branch was available, precluding a double-barrel STA strategy. The video details graft tailoring, temporary clipping, end-to-side anastomoses, and bypass sequencing. Intraoperative indocyanine green angiography and Doppler ultrasonography were used to confirm bypass patency and robust distal flow through both reconstructions. To preserve proximal perforators, distal trapping only was performed, allowing progressive aneurysm thrombosis while maintaining distal perfusion. Postoperative imaging demonstrated near-complete aneurysm thrombosis with preserved distal MCA flow. A flow-guided dual revascularization strategy can provide a reliable microsurgical solution for complex fusiform MCA bifurcation aneurysms involving both M2 trunks, emphasizing physiologic donor selection and perforator-preserving aneurysm exclusion. - Source: PubMed
Publication date: 2026/03/30
Starnoni DanieleGolub DanielleDehdashti Amir R - Fusiform intracranial aneurysms (IAs) can be challenging to treat, especially when ruptured. Clip trapping and bypass is an important treatment modality for complex IAs not amenable to endovascular approaches (i.e., stent-assisted coiling, flow diversion), which can be limited by low occlusion rates and anatomical constraints (e.g., tortuosity, proximity to branching vessels). Here we highlight the treatment considerations and technical steps for clip trapping and intracranial bypass of a previously ruptured middle cerebral artery fusiform aneurysm. A 76-year-old man with a history of atrial fibrillation presented with subacute progressive headaches and lower-extremity weakness one month after admission elsewhere for reported hypertensive hemorrhage. Imaging demonstrated a right-sided 4.3 × 3.0-mm fusiform IA involving the proximal nondominant anterior temporal M2 artery and subacute bilateral basal ganglia strokes, presumably from vasospasm; prior imaging showed a right peri-sylvian hemorrhage. He was neurologically intact, except for diffusely weakened lower extremities (4/5). Endovascular treatment options were dismissed because of small vessel size and his hesitance toward dual-antiplatelet therapies. Vessel sacrifice was not selected because of the stroke risk. A clip-trapping and flow-preserving bypass was selected for treatment, with superficial temporal artery (STA)-M2 selected because there was a large frontal STA donor branch and nondominant M2 recipient vessel. After uneventful surgery, postoperative imaging demonstrated complete aneurysm occlusion, a patent bypass filling the temporal M2, and no new strokes. The patient returned to his prehemorrhage baseline by 2-month follow-up. Flow-preserving cerebral bypass remains an important skill for the management of complex IAs in properly selected patients in the endovascular era. - Source: PubMed
Publication date: 2025/09/30
de Lotbiniere-Bassett Madeleine PCouldwell William TRennert Robert C - Cellular senescence is a critical process involved in aging and related disorders, yet the molecular triggers of early senescence remain elusive. Here, we identify DNA methyltransferase 1 (DNMT1) downregulation as a key trigger of early senescence and establish serine protease inhibitor Kunitz type 2 (SPINT2) as its critical downstream effector. Using replicative and oxidative stress-induced senescence models of primary human diploid fibroblast, we observed persistent upregulation of SPINT2 and inverse downregulation of DNMT1, preceding senescence-associated β-galactosidase activity, a conventional senescence marker. Pharmacological inhibition and siRNA-mediated knockdown of DNMT1 significantly increased SPINT2 expression and induced senescence, showing mitigated effects by SPINT2 knockdown. Furthermore, SPINT2 overexpression alone induced senescence. Methylation-specific sequencing identified four CpG sites in SPINT2 promoter, that became hypomethylated at early transition of senescence and upon DNMT1 suppression. Functional analyses revealed that DNMT1-mediated SPINT2 expression induced c-Met inhibition, triggering senescence. Transcriptomic profiling identified 17 commonly deregulated c-Met signaling genes in both senescence models, with COL27A1, STAM2, and CBL validated as key downstream targets of SPINT2/c-Met signaling. These findings establish DNMT1-mediated SPINT2 upregulation as a novel epigenetic mechanism driving senescence initiation via c-Met inhibition, providing insights into the early stage of senescence and potential therapeutic targets for aging-related diseases. - Source: PubMed
Publication date: 2025/08/20
Sim Min SeokByun Hae-OkMin SeongkiHong JiwonLim Su BinChoi Kyoung SookYoon Gyesoon - Cushing's disease is a rare endocrine disorder characterized by excessive endogenous glucocorticoid production, primarily resulting from adrenocorticotropic hormone-secreting pituitary neuroendocrine tumors (ACTH-PitNETs). This study investigated the expression of several genes implicated in the development of ACTH-PitNETs, including EGFR, USP8, CABLES1, USP2, STAM2, VPS28, HDAC2, IL-6, SMARCA4, WEE1, CDKN2A, CCND1, NR4A1, NEUROD1, and RIPK1. The methylation levels of the USP8 and CDKN2A genes were also assessed for insights into their regulatory mechanisms.Formalin-fixed paraffin-embedded pituitary tumor tissue samples from 32 patients diagnosed with ACTH-PitNET and 15 anterior pituitary tissue samples were analyzed. Gene expression was analyzed through quantitative reverse transcription polymerase chain reaction, while methylation was examined through methylation-specific polymerase chain reaction. All data were analyzed with IBM SPSS Statistics 21. The relationships among gene expressions were assessed using principal component analysis.The expression of CABLES1, NR4A1, CCND1, NEUROD1, USP2, and WEE1 differed significantly between the patient and control groups. Additionally, significant correlations were observed between the levels of RIPK1, SMARCA4, and USP2 and pre-operative cortisol levels; WEE1 expression and pre-operative ACTH levels; CDKN2A expression and urinary cortisol levels; CABLES1, NEUROD1, SMARCA4, and STAM2 expression and post-operative cortisol levels at 48 h. CCND1 expression was correlated with adenoma size, while WEE1 expression was linked to remission status. Notably, the CDKN2A gene displayed partial methylation, whereas the USP8 gene was fully unmethylated.The altered expression levels of the USP2, CABLES1, CDKN2A, and WEE1 may be closely associated with the development of ACTH-PitNETs. Notably, WEE1 emerged as a target gene for predicting clinical remission in patients with Cushing's disease. - Source: PubMed
Publication date: 2025/07/30
Kayacan SeraGazioglu NurperiOrhan CerenComunoglu NilKadioglu PinarTanriover NecmettinUysal OmerKaya Dagistanli FatmaOzturk Melek - The secretion of programmed death ligand 1 (PD-L1) via small extracellular vesicles (sEVs) endows this immune checkpoint protein with diverse and systemic roles. This intercellular communication mediated by sEV PD-L1 not only fosters a pro-tumorigenic niche but also induces systematic immunosuppression. Revealing the intricate mechanisms underlying sEV PD-L1 secretion is essential for understanding tumor pathology and developing targeted therapies. Here, we demonstrated the specialization and collaboration among members of the endosomal sorting complex required for transport-0 (ESCRT-0) family in regulating sEV PD-L1 secretion in oral squamous cell carcinoma (OSCC). Mechanistically, STAM2, not STAM1, directly binds cell surface PD-L1, followed by recruiting HRS to initiate the biogenesis of PD-L1 sEVs. Specifically, STAM2 binds the functional domains of PD-L1 and HRS through the VHS and ITAM domains respectively, acting as a molecular bridge between PD-L1 and HRS. Therefore, our study delineated the sequential participation of different ESCRT-0 members during sEV PD-L1 secretion and highlighted the pivotal role of STAM2 in orchestrating this process, providing important insights into diseases with aberrant PD-L1 secretion, such as OSCC. - Source: PubMed
Publication date: 2025/06/18
Wang Xiao-LeXia Hou-FuChen Zhuo-KunWang Kui-MingZhang WeiChen Gang