Human Apo-AI _ApoA1 Protein Vector: HEK294
- Known as:
- Human Apo-AI _ApoA1 Protein Vector: HEK294
- Catalog number:
- 10014-H01H
- Product Quantity:
- 50μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human Apo- _ApoA1 Protein Vector: HEK294
Related genes to: Human Apo-AI _ApoA1 Protein Vector: HEK294
- Gene:
- APOA1 NIH gene
- Name:
- apolipoprotein A1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
- Gene:
- APOM NIH gene
- Name:
- apolipoprotein M
- Previous symbol:
- -
- Synonyms:
- ApoM, G3a, NG20
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-02
- Date modifiied:
- 2016-10-05
- Gene:
- TNFRSF10A NIH gene
- Name:
- TNF receptor superfamily member 10a
- Previous symbol:
- -
- Synonyms:
- DR4, Apo2, TRAILR-1, CD261, TRAILR1
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2018-01-25
- Gene:
- TNFSF10 NIH gene
- Name:
- TNF superfamily member 10
- Previous symbol:
- -
- Synonyms:
- TRAIL, Apo-2L, TL2, CD253
- Chromosome:
- 3q26
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2017-03-02
Related products to: Human Apo-AI _ApoA1 Protein Vector: HEK294
Related articles to: Human Apo-AI _ApoA1 Protein Vector: HEK294
- Adipose-derived stem cells (ADSCs) are readily harvestable, tumour-homing cells that have been engineered as vehicles for antitumour agents. TNF-related apoptosis-inducing ligand (TRAIL) selectively triggers apoptosis in many cancer cells through death receptors DR4/DR5, while sparing most healthy cells. To date, only human TRAIL has been studied in such delivery systems; a fully homologous rat model (rat TRAIL delivered by rat ADSC) has not been tested, despite being essential for future syngeneic in vivo studies. - Source: PubMed
Publication date: 2026/09/15
Pascal WiktorGotowiec MateuszSmoliński AntoniWłodarski Paweł K - Delayed graft function after kidney transplant is associated with increased acute rejection rates and poorer long-term outcomes. It is significantly more prevalent in recipients of deceased than living donor kidneys due to increased ischemia-reperfusion injury associated with prolonged warm and cold ischemic times. Although specific immune populations are associated with ischemia-reperfusion injury and delayed graft function, the precise cellular circuits distinguishing deceased from living donor transplants, as well as the donor and recipient-derived immune programs involved in early immunological responses, have not been defined at cellular resolution. - Source: PubMed
Publication date: 2026/09/22
Mak Martin LMurphy Julia MMathews Jessica ASu ShenghuiKonvalinka AnaEpelman SlavaCrome Sarah Q - Spleen tyrosine kinase (Syk) regulates immune responses and has been implicated in haematopoietic and epithelial cancers. Although our previous studies showed that Syk modulates keratinocyte differentiation and UVB-induced inflammation, its role in UVB-related cutaneous squamous cell carcinoma (cSCC) remains unclear. Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis in cancer cells and is expressed in healthy skin but reduced in non-melanoma skin cancers and sun-exposed skin. This study investigated the role of Syk in cSCC and TRAIL-induced apoptosis. Immunohistochemistry revealed elevated phosphorylated and total Syk levels in SCC tissues compared with normal skin. In SCC12 cells, TRAIL induced dose-dependent apoptosis, which was enhanced by pharmacological Syk inhibition or Syk silencing. Combination treatment with TRAIL and Syk inhibitors increased annexin V positivity and cleavage of caspase-3, PARP1 and Bid, accompanied by reduced Mcl-1 expression. Mechanistically, TRAIL induced Src and Syk phosphorylation. TRAIL-induced Syk activation was suppressed by Src inhibition but not by EGFR inhibition, indicating that Syk activation is Src-dependent but EGFR-independent in this pathway. Syk inhibition further reduced TRAIL-activated Akt and MAPK signalling, while Akt activation may play a role in regulating SCC12 survival. These results suggest that targeting Syk sensitizes TRAIL-mediated apoptosis and may offer a promising therapeutic strategy for treating cutaneous SCC. - Source: PubMed
Lu Po-HsuanChiu Ling-YaWang Jen-YuHsiao Pa-FanLu Ping-HsunHuang Yi-TingCheng Yi-TingWu Nan-Lin - Rheumatoid arthritis (RA) is closely associated with genetic factors, but there is still a lack of ideal biomarkers for its early diagnosis and precise intervention. To investigate the diagnostic value and synovial cell function of miR-7641 in RA, and its mechanistic link to TNFSF10. A case-control study was conducted with 152 RA patients and 152 matched asymptomatic first-degree relatives. Serum miR-7641 and TNFSF10 levels were quantified by qRT-PCR. Diagnostic accuracy was assessed via logistic regression and ROC analysis. In MH7A cells, miR-7641 mimic/inhibitor transfection was performed, followed by assessments of proliferation (CCK-8), inflammatory cytokines (ELISA), and target interaction (dual-luciferase assay). Rescue experiments involved co-transfection of the miR-7641 mimic and a TNFSF10 overexpression plasmid. Serum miR-7641 was downregulated in RA patients and identified as an independent protective factor with high diagnostic accuracy (AUC = 0.902). In MH7A cells, miR-7641 overexpression suppressed proliferation and reduced IL-6, IL-1β, and TNF-α secretion. TNFSF10 was confirmed as a direct target, with its expression negatively correlating with miR-7641 in serum samples. Importantly, TNFSF10 overexpression rescued the inhibitory effects of miR-7641 on proliferation and cytokine production. This study identifies serum miR-7641 as a potential diagnostic biomarker for RA. In an immortalized synovial cell model, miR-7641 exerts protective effects by targeting TNFSF10 to inhibit proliferation and inflammation. Future studies in primary cells and in vivo models are required to validate these findings and explore downstream signalling mechanisms. - Source: PubMed
Publication date: 2026/09/18
Zhang YuchenChen HuijinLiang HongmingZhang JinxiangWan Jian - Tumor necrosis factor-alpha (TNF-α) inhibitors are effective biologics for immune-mediated inflammatory diseases, including plaque psoriasis and inflammatory bowel disease (IBD). However, time-course peripheral blood transcriptomic changes during treatment remain poorly characterized. To characterize transcriptomic changes associated with TNF-α inhibitor treatment, we profiled blood transcriptomics at three time points in 86 patients with plaque psoriasis receiving TNF-α inhibitor. We identified 3,351 time-course drug-response genes (DRGs), enriched in immune signaling and cell activation pathways and expressed in psoriatic skin lesion and blood. Among them, 259 genes showed differentially expressed between at least one pair of the three sampling time points and 962 were shared between psoriasis and IBD. TNF-α inhibitor responders showed higher expression of OLIG1, LRRK1, and KSR1, and lower expression of TNFAIP3 and MPP7 than non-responders. We identified a "red" gene co-expression module negatively correlated with treatment outcome and enriched in inflammation and TNF-related pathways. High expression of TNFSF10 (top hub gene of the "red" module) was associated with poor outcome. By week 2, the red module's co-expression pattern changed significantly in responders but not in non-responders. This study characterizes time-course peripheral blood transcriptional programs of TNF-α inhibitor therapy in plaque psoriasis. - Source: PubMed
Publication date: 2026/09/09
Xia ZhijieLiu LunfeiWang TaoXue YiLiu JipengYu DianheHu HonghuaChen QiChu XiaomengPeng RuyiLiu LeiWang JinyanCheng HaoFang HongZheng MinYin XianyongRen Yunqing