Skin Lysate
- Known as:
- Skin Lysate
- Catalog number:
- 1376
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- Skin Lysate
Related genes to: Skin Lysate
- Gene:
- CCL27 NIH gene
- Name:
- C-C motif chemokine ligand 27
- Previous symbol:
- SCYA27
- Synonyms:
- ALP, ILC, CTACK, skinkine, ESkine, PESKY, CTAK
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-30
- Date modifiied:
- 2016-10-05
Related products to: Skin Lysate
Related articles to: Skin Lysate
- Cardiovascular diseases (CVDs) encompass a group of diseases that affect the heart and/or blood vessels, making them the leading cause of global mortality. In our study, we performed proteome-wide Mendelian randomization (MR) and colocalization analyses to identify novel therapeutic protein targets for CVDs and evaluate the potential drug-related protein side effects. We conducted a comprehensive proteome-wide MR study to assess the causal relationship between plasma proteins and the risk of CVDs. Summary-level data for 4907 circulating protein levels were extracted from a large-scale protein quantitative trait loci (pQTL) study involving 35,559 individuals. Additionally, genome-wide association study (GWAS) data for CVDs were extracted from the UK Biobank and the Finnish database. Colocalization analysis was utilized to identify causal variants shared between plasma proteins and CVDs. Finally, we conducted a comprehensive phenome-wide association study (PheWAS) using the R10 version of the Finnish database. This study was aimed at examining the potential drug-related protein side effects in the treatment of CVDs. A total of 2408 phenotypes were included in the analysis, categorized into 44 groups. The research findings indicate the following associations: (1) In coronary artery disease (CAD), the plasma proteins A4GNT, COL6A3, KLC1, CALB2, KPNA2, MSMP, and ADH1B showed a positive causal relationship (-fdr < 0.05). LAYN and GCKR exhibited a negative causal relationship (-fdr < 0.05). (2) In chronic heart failure (CHF), PLG demonstrated a positive causal relationship (-fdr < 0.05), while AZGP1 displayed a negative causal relationship (-fdr < 0.05). (3) In ischemic stroke (IS), ALDH2 exhibited a positive causal relationship (-fdr < 0.05), while PELO showed a negative causal relationship (-fdr < 0.05). (4) In Type 2 diabetes (T2DM), the plasma proteins MCL1, SVEP1, PIP4K2A, RFK, HEXIM2, ALDH2, RAB1A, APOE, ANGPTL4, JAG1, FGFR1, and MLN demonstrated a positive causal relationship (-fdr < 0.05). PTPN9, SNUPN, VAT1, COMT, CCL27, BMP7, and MSMP displayed a negative causal relationship (-fdr < 0.05). Colocalization analysis conclusively identified that AZGP1, ALDH2, APOE, JAG1, MCL1, PTPN9, PIP4K2A, SNUPN, and RAB1A share a single causal variant with CVDs (PPH3 + PPH4 > 0.8). Further phenotype-wide association studies have shown some potential side effects of these nine targets (-fdr < 0.05). This study identifies plasma proteins with significant causal associations with CVDs, providing a more comprehensive understanding of potential therapeutic targets. These findings contribute to our knowledge of the underlying mechanisms and offer insights into potential avenues for treatment. - Source: PubMed
Publication date: 2025/02/21
Fan MaoxiaLi NaHuang LibinChen ChenDong XueyanGao Wulin - Hypertrophic scars result from abnormal healing following skin injuries. - Source: PubMed
Li YanqiZhang YankunWang WanchaoWang YugeAi Hongmei - Aging increases disease susceptibility and reduces vaccine responsiveness, highlighting the need to better understand the aging immune system and its clinical associations. Studying the human immune system, however, remains challenging due to its complexity and significant inter-individual variability. - Source: PubMed
Publication date: 2025/01/24
Riemann LennartGutierrez RodrigoOdak IvanBarros-Martins JoanaRoesner Lennart MLeon Lara XimenaFalk ChristineSchulz Thomas FHansen GesineWerfel ThomasFörster Reinhold - Exposure to ionizing radiation (IR), both low-LET (e.g., X-rays, γ rays) and high-LET (e.g., heavy ions), increases the risk of gastrointestinal (GI) cancer. Previous studies have linked IR-induced GI cancer to cellular senescence associated secretory phenotype (SASP) signaling. This study explores the potential of senolytic therapy to mitigate IR-induced GI carcinogenesis. Male mice were exposed to γ and Si-ions (69 keV/μm) IR. Two months later, they were treated with the senolytic agent ABT-263 orally for 5 days/week until euthanasia, followed by tumor counting and biospecimen collection at five months post-exposure. Tumors were classified as adenoma or carcinoma by a pathologist. Serum cytokine levels were measured, and the markers of senescence (p16), SASP (IL6), and oncogenic β-catenin signaling were assessed using immunostaining of intestinal tissue. Both low- and high-LET radiation exposure led to an increased frequency of adenoma and carcinoma in mice, accompanied by increased cellular senescence, acquisition of SASP, and overexpression of BCL-XL protein in a subset of these cells. Furthermore, administration of ABT-263 resulted in the elimination of senescent/SASP cells, a decrease in pro-inflammatory cytokines (TNFRSF1B, CCL20, CXCL4, P-selectin, CCL27, and CXCL16) at the systemic level, and downregulation of β-catenin signaling that coincided with decreased GI cancer development. This study suggests a link between IR-induced senescent/SASP cell accumulation and GI cancer development. It also shows that the senolytic agent ABT-263 can regulate IR-induced inflammatory cytokines and carcinogenic mediators both systemically and in intestinal tissue. These findings support the potential of senolytic intervention to reduce IR-induced GI cancer risk. - Source: PubMed
Publication date: 2025/01/08
Kumar KamendraMoon Bo-HyunKumar SantoshAngdisen JerryKallakury Bhaskar V SFornace Albert JSuman Shubhankar - The rapid approval of SARS-CoV-2 mRNA lipid nanoparticle (LNP) vaccines indicates the versatility of mRNA LNPs in an urgent vaccine need. However, the mRNA vaccines do not induce mucosal cellular responses or broad protection against recent variants. To improve cross-protection of mRNA vaccines, here we engineered a pioneered mRNA LNP encapsulating with mRNA constructs encoding cytokine adjuvant and influenza A hemagglutinin (HA) antigen for intradermal vaccination. The adjuvant mRNA encodes a novel fusion cytokine GIFT4 comprising GM-CSF and IL-4. We found that the adjuvanted mRNA LNP vaccine induced high levels of humoral antibodies and systemic T cell responses against heterologous influenza antigens and protected immunized mice against influenza A viral infections. Also, the adjuvanted mRNA LNP vaccine elicited early germinal center reactions in draining lymph nodes and promoted antibody-secreting B cell responses. In addition, we generated another adjuvant mRNA encoding CCL27, which enhanced systemic immune responses. We found the two adjuvant mRNAs both showed effective adjuvanticity in enhancing humoral and cellular responses in mice. Interestingly, intradermal immunizations of GIFT4 or CCL27 mRNA adjuvanted mRNA LNP vaccines induced significant lung tissue-resident T cells. Our findings demonstrate that the cytokine mRNA can be a promising adjuvant flexibly formulated into mRNA LNP vaccines to provoke strong immunity against viral variants. - Source: PubMed
Publication date: 2024/12/22
Wei LaiZhu WandiDong ChunhongKim Joo KyungMa YaoDenning Timothy LKang Sang-MooWang Bao-Zhong