CXCL12 _ SDF1 (alpha)
- Known as:
- CXCL12 _ SDF1 (a)
- Catalog number:
- GTX29798
- Product Quantity:
- 10 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CXCL12 _ SDF1 (alpha)
Related genes to: CXCL12 _ SDF1 (alpha)
- Gene:
- A4GNT NIH gene
- Name:
- alpha-1,4-N-acetylglucosaminyltransferase
- Previous symbol:
- -
- Synonyms:
- alpha4GnT
- Chromosome:
- 3q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-07-12
- Date modifiied:
- 2016-10-05
- Gene:
- ABCB5 NIH gene
- Name:
- ATP binding cassette subfamily B member 5
- Previous symbol:
- -
- Synonyms:
- EST422562, ABCB5beta, ABCB5alpha
- Chromosome:
- 7p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2016-10-05
- Gene:
- AGPAT1 NIH gene
- Name:
- 1-acylglycerol-3-phosphate O-acyltransferase 1
- Previous symbol:
- -
- Synonyms:
- LPAAT-alpha
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-07
- Date modifiied:
- 2016-10-05
- Gene:
- AKR1C4 NIH gene
- Name:
- aldo-keto reductase family 1 member C4
- Previous symbol:
- CHDR
- Synonyms:
- DD4, HAKRA, C11, 3-alpha-HSD, CDR, MGC22581
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-08-26
- Date modifiied:
- 2016-06-03
- Gene:
- ARHGEF6 NIH gene
- Name:
- Rac/Cdc42 guanine nucleotide exchange factor 6
- Previous symbol:
- MRX46
- Synonyms:
- alphaPIX, Cool-2, KIAA0006, alpha-PIX, Cool2
- Chromosome:
- Xq26.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-27
- Date modifiied:
- 2016-10-05
Related products to: CXCL12 _ SDF1 (alpha)
Related articles to: CXCL12 _ SDF1 (alpha)
- The chemokine CXCL12, as a pivotal immune regulator, plays a crucial role in teleost fish against bacterial infection, but current research on its specific mechanisms remains scarce. This study systematically identified two copies of the CXCL12 in turbot (Scophthalmus maximus) (SmCXCL12a and SmCXCL12b), investigated their expression patterns, and revealed their immune functions and antibacterial mechanisms. Firstly, phylogenetic and syntenic analyses indicated that the SmCXCL12a/b were relatively conserved and exhibited high homology with orthologs in other teleost fish, including Japanese flounder (Paralichthys olivaceus). Secondly, of the nine tissues examined in healthy fish, the highest expression level of SmCXCL12a was observed in the kidney, while the highest expression level of SmCXCL12b was detected in the skin. Following infection with Aeromonas salmonicida, significant differential expression of SmCXCL12a and SmCXCL12b was observed in the gills, intestines, and skin. Additionally, both rSmCXCL12a and rSmCXCL12b exhibited chemotactic activity toward kidney macrophages, splenic leukocytes, and peripheral blood leukocytes. Notably, the growth of Escherichia coli and Staphylococcus aureus was inhibited by rSmCXCL12a and rSmCXCL12b. In addition, rSmCXCL12a and rSmCXCL12b exhibited significant binding capacity to multiple Gram-positive and Gram-negative bacteria, with their binding patterns toward bacterial surface substances such as PGN, LPS, LTA, and Poly(I:C). Therefore, it was speculated that they might exert antibacterial functions by recognizing bacterial surface substances. Furthermore, the agglutination properties of rSmCXCL12a and rSmCXCL12b toward various bacteria suggested their capacity to engage with bacterial surface substances. Finally, it was observed that rSmCXCL12a/b could alter the permeability of bacterial cell membranes, resulting in propidium iodide (PI) influx. Meanwhile, changes in membrane potential were detected in DiOC(3) experiments. Hence, it was hypothesized that one of its antibacterial mechanisms could be membrane attack. To conclude, this research thoroughly elucidated the function of the two copies of SmCXCL12 in immune response and antibacterial mechanisms during bacterial infection, providing a theoretical basis for the application of chemokines in the prevention and control of bacterial fish diseases. - Source: PubMed
Publication date: 2026/04/16
Zhang XiaoxuWang BeibeiLiu YiyingZhang PeiChen ChonghuiLi ChaoFu Qiang - In colitis-associated colorectal cancer (CAC), chronic inflammation is the primary driver of tumorigenesis. A critical event in this process is the massive recruitment of neutrophils, which, while part of the host defense, can paradoxically fuel cancer progression. Excessive neutrophil infiltration contributes to sustained mucosal damage through the release of pro-inflammatory mediators and shapes a tumor-promoting microenvironment. Despite their recognized role, therapeutic strategies specifically targeting pathogenic neutrophil recruitment in CAC are limited. Thlaspi arvense (TA), a traditional medicinal plant, possesses purported anti-inflammatory properties, suggesting its potential utility against CAC. Therefore, this study was designed to evaluate the efficacy of TA in preventing CAC and to delineate its mechanism of action, particularly its impact on neutrophil-driven inflammation. - Source: PubMed
Publication date: 2026/04/17
Wang ZiweiWang WenkaiWang ChaoweiDong BijinSun YunchuanHe XinyingBi LingWang Yan - Microvessels within atherosclerotic plaques are crucially involved in disease progression. Here, we generated a transcriptomic atlas of human atherosclerosis at single-cell resolution, encompassing 17,367 vascular endothelial cells (VECs) from five scRNA-seq studies, and verified key morphological characteristics using histology. SULF1 arterial endothelial cells (ArtECs) represented the primary subcluster undergoing endothelial-to-mesenchymal transition (EndMT). Capillary-like endothelial cells (CapECs) were identified as primary mediators of angiogenesis, and a trajectory model illustrated the transition between tip and stalk cells, with subclusters of ArtECs and CapECs predominantly expressing CXCL12, thereby driving the CXCL12/CXCR4 signaling axis. The largest plaque EC cluster, exhibiting the most heterogeneity, was found among post-capillary venule endothelial cells (VenECs), particularly ACKR1NR2F2 VenECs, which displayed distinct inflammatory transcriptional signatures characterized by adhesion molecules and chemokines. Overall, this atlas of atherosclerosis underscores endothelial heterogeneity and identifies SULF1 ArtECs and VenECs as potential therapeutic targets for EndMT and leukocyte recruitment, respectively. - Source: PubMed
Publication date: 2026/04/17
Wu YanzhaoXue ZhiweiSun TaoYu YindaLiang XiangjunXing WenchenMu FeiyuZhang ZhihanLv MeilinLing LuHan MengtaoCheng LianGisterå AntonWang Donghai - Pancreatic ductal adenocarcinoma (PDAC) diagnoses are often accompanied by a number of physical and psychological symptoms, including anxiety and depression. As a result, many patients are prescribed anxiolytics such as benzodiazepines that have unintended effects on the tumor. Previous work from our lab has highlighted that structural differences between benzodiazepine compounds may be responsible for different clinical outcomes influenced by their effects on cancer-associated fibroblasts (CAFs) within the PDAC tumor microenvironment (TME). Here, we demonstrate that the commonly prescribed N-substituted triazolobenzodiazepine alprazolam (ALP) abrogates the production of proinflammatory cytokines including CCL2, CXCL12, IL6, and IL8 in human CAFs. This phenotype is unique only to azole-containing benzodiazepines, including midazolam. The ability of ALP to regulate proinflammatory cytokine production is maintained in vivo, as ALP-treated mice bearing pancreatic tumors exhibited reductions in IL6 within the tumor interstitial fluid. Mechanistically, an unbiased phosphoproteomic approach revealed that ALP abrogates TLR4-mediated cytokine production in CAFs. These findings cumulatively support that ALP dampens CAF-mediated inflammatory signaling within the PDAC TME. - Source: PubMed
Publication date: 2026/04/17
Reavis Hunter DChaubey Aditi HSmythers Amanda LTisdale Arwen ATracz AmandaDimeck Alphonse NMaraszek Kathryn ECortes Gomez EduardoPaulo Joao ADasgupta SubhamoyGygi Steven PFeigin Michael E - The regenerative capacity of adult bone relies on the rapid activation and lineage engagement of skeletal stromal and progenitor cells (SSPCs). While signaling pathways that regulate these processes have been extensively studied, the epigenetic mechanisms that constrain progenitor activation and lineage permissiveness during adult bone repair remain poorly defined. Disruptor of telomeric silencing 1 like (Dot1L), the sole histone methyltransferase responsible for H3K79 methylation, is essential for skeletal development, yet its function in adult skeletal regeneration has not been established. Here, we identify Dot1L as a key epigenetic regulator that limits the early regenerative response to bone injury. Genetic reduction of Dot1L activity in the Prrx1 mesenchymal lineage enhances stromal progenitor activation, proliferative engagement, and differentiation capacity, revealing a previously unrecognized role for Dot1L in restraining progenitor responsiveness in adult bone. Notably, acute pharmacologic inhibition of Dot1L using the selective H3K79 methyltransferase inhibitor EPZ-5676 similarly enhances early progenitor activation, indicating that reduced Dot1L enzymatic activity is sufficient to modulate regenerative engagement. At the cellular level, reduced Dot1L activity expands injury-responsive Cxcl12 stromal populations and increases osteogenic progenitor abundance following injury. Consistent with these cellular changes, Dot1L reduction is associated with accelerated early bone formation Collectively, these findings position Dot1L as an epigenetic gatekeeper that constrains early progenitor activation during the initial phase of adult skeletal repair. - Source: PubMed
Publication date: 2026/04/09
Stetsiv MartaDauphinee DrewAbdulsalam SakinahPrabhu ShagunTress AlexanderCobb KerrySanjay ArchanaGuzzo Rosa M