SH3KBP1 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- SH3KBP1 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00030011-T01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- SH3KBP1 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: SH3KBP1 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- SH3KBP1 NIH gene
- Name:
- SH3 domain containing kinase binding protein 1
- Previous symbol:
- -
- Synonyms:
- CIN85
- Chromosome:
- Xp22.12
- Locus Type:
- gene with protein product
- Date approved:
- 2000-12-14
- Date modifiied:
- 2016-10-05
Related products to: SH3KBP1 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: SH3KBP1 293T Cell Transient Overexpression Lysate(Denatured)
- Glioblastoma (GBM) is an aggressive brain tumor characterized by rapid growth and infiltration. New therapies are desperately needed to improve GBM patient outcomes. Intra-tumoral heterogeneity is a common driver of failure for novel GBM treatments, and many preclinical studies rely on cell lines established from the tumor core. As a result, they fail to characterize the infiltrative tumor cells, which remain post-surgery and ultimately drive tumor recurrence. - Source: PubMed
Publication date: 2026/07/10
Porter HarryMulhall KayleyShah MariaVinohar Jeffy JosephKaradimas Konstantinos-PanagiotisMistry ShaylenDeacon SimonHaque FarhanaBakker EmyrBoocock David JCoveney ClareLayfield RobertRahman RumanMcCrorie Phoebe - Autism Spectrum Disorder (ASD) is a heterogeneous neurodevelopmental condition characterized by impairments in social communication and restricted, repetitive behaviors. Increasing evidence suggests that immune dysregulation may be present in a subset of individuals with neurodevelopmental disorders, although its role in ASD remains incompletely understood. We report two male patients with ASD, neurodevelopmental delay, immune dysregulation, and congenital cardiac anomalies. Genetic analysis using chromosomal microarray (CMA) identified distinct copy number variants on the X chromosome in each case. In patient 1, a duplication of the Xq28 region encompassing the gene was identified, consistent with MECP2 duplication syndrome, a well-established cause of neurodevelopmental impairment and recurrent infections. In this case, the clinical presentation was comparatively milder than typically described, highlighting phenotypic variability within this condition. In patient 2, a hemizygous deletion at Xp22.12 partially involving the gene was detected and classified as a variant of uncertain significance (VUS). The patient presented with recurrent respiratory infections, impaired humoral immune responses, reduced B-cell counts, and neurodevelopmental impairment. This observation broadens the limited clinical spectrum associated with ariants and may aid future assessment of their clinical relevance, although a causal relationship remains unproven. Together, these observations emphasize the value of comprehensive genetic testing in individuals with complex neurodevelopmental and systemic presentations and support consideration of immunological evaluation in selected patients with ASD who present with recurrent infections, allergic disease, or additional phenotypic features suggestive of inborn errors of immunity. - Source: PubMed
Publication date: 2026/06/15
Marin-Llobet ArnauHernando-Davalillo CristinaBaide-Mairena HeidyLlobet-Agullo PilarFornes Garcia NeusPerez-Herrera VeronicaBaro-Serrano Anna - Ovarian cancer (OC) remains the most lethal gynecological malignancy, with profound tumor microenvironment (TME) heterogeneity contributing to the suboptimal clinical response to immune checkpoint inhibitors (ICIs). Therefore, delineating the metabolic heterogeneity of T cells within the TME is imperative for identifying precise prognostic biomarkers and refining individualized immunotherapeutic strategies. - Source: PubMed
Publication date: 2026/04/24
Tian HuadongLiu XiaotongWang GuojiaoWang ZimoLuo Yuexi - Aberrant lipid metabolism is a hallmark of hepatocellular carcinoma (HCC), yet the regulatory mechanisms governing lipid droplet (LD) dynamics and their contribution to tumor progression remain poorly understood. Here, we developed an ultrasensitive phosphoproteomic platform using high-affinity HPDA@Ti nanospheres to map LD-associated phosphorylation events across six HCC cell lines. By correlating phosphoproteomic signatures with LD morphology, we identified distinct regulatory signatures associated with LD size and abundance. Functional perturbation screens identified two distinct phosphoprotein modules controlling LD size: silencing , , , , and reduced LD size in Huh1 cells, whereas silencing , , , , , and enlarged LDs in Huh7 cells. Notably, we identified EPB41L3 as a critical metabolic-metastatic link; its loss decreased LD size and accelerated HCC migration and invasion, correlating with poor clinical prognosis. Crucially, we identified five key phosphorylation sites on EPB41L3 essential for its function; substituting these with alanine completely abolished its regulatory control over both LD size and HCC metastatic potential. Together, these findings delineate a phosphorylation-based regulatory network controlling the LD architecture and metastatic potential in HCC. Our study not only identifies potential therapeutic targets but also establishes a generalizable phosphoproteomic framework for interrogating lipid signaling in cancer metabolism. - Source: PubMed
Publication date: 2026/05/29
Mao Jian-WenXia YanLuo Xue-YangWang ShupeiGong JingyiXu JindianChen WeiweiWu JiaqiLi ZimengLuo JiahuiZhang HongyeLu QingWu DuojiaoWu Wei-ZhongWang JiaxiHuang Li-Hao - USP8 is one of the members of ubiquitin-specific proteases deconjugating ubiquitin from target proteins. Besides USP6, it can be involved in tumorigenesis of mesenchymal neoplasms by binding to an activating fusion partner. Until now, USP8 fusion genes have been reported in calcified chondroid mesenchymal neoplasms, an inflammatory myofibroblastic tumor, a cardiac neoplasm, and a retroperitoneal sarcoma. In this study, we describe the clinicopathologic and genetic/epigenetic features of 7 USP8-associated tumors. The cohort included 5 male patients aged between 2 and 11 years, and 2 female patients aged 38 and 52 years. Lesions arose in the tongue, finger, hallux, arm, thoracic wall, right ventricle, and leg. Five neoplasms were resected. One was a recent case; the others were without evidence of disease after 0.5 to 3 years. Two lesions were only biopsied, 1 was a recent case and the other had no signs of progression after 4 years. Histology showed nodular or infiltrative lesions comprising bland-looking myofibroblastic spindle cells arranged in mainly short fascicles. The cellularity was variable, and the background was myxoid and/or collagenous. An inflammatory reaction was variably seen. One lesion, however, had features of a chondroid calcified mesenchymal neoplasm. Using RNA-sequencing, the following fusion partners of USP8 were found: SH3KBP1, RASA1, PDGFRA, CRK, PTPN11, and FARP1. Based on RNA-expression analysis, the 2 cases analyzed had a profile of nodular fasciitis; whereas using the Heidelberg Sarcoma Classifier, all cases had a similar methylation profile apart from other soft tissue tumor entities, suggesting that they form a separate group but are closely related to USP6-associated lesions. In conclusion, we broadened the spectrum of USP8-associated mesenchymal lesions in superficial, deep soft tissues and viscera (heart). Almost all lesions in this series displayed a myofibroblastic phenotype and harbored variable USP8 fusion partners. RNA-expression profiling indicated partial clustering with nodular fasciitis, suggesting some biological similarity. However, DNA methylation analysis consistently showed that these tumors formed a distinct epigenetic group, separate from both nodular fasciitis and inflammatory myofibroblastic tumors. Taken together, these findings support the concept of a USP8-rearranged myofibroblastic neoplasm as a potentially distinct entity, but the precise relationship with nodular fasciitis and inflammatory myofibroblastic tumor remains uncertain. Further studies integrating morphology, epigenetics, and transcriptomics are needed to clarify this relationship. - Source: PubMed
Publication date: 2025/12/09
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