CXCL12 _ SDF1 (alpha)
- Known as:
- CXCL12 _ SDF1 (a)
- Catalog number:
- TP201
- Product Quantity:
- 0.2 mg
- 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)
- 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 - Successful pregnancy requires exquisite balance: the placenta must invade just enough to access maternal blood but not so deep it remains attached at birth. Disrupting this balance causes life-threatening pregnancy complications, for which treatments remain limited. Animal models are desperately needed to discover mechanisms underlying balanced uteroplacental development and how pregnancy complications arise, but this is hampered by the view that mouse placentation lacks human characteristics such as extensive trophoblast invasion and targeting of uterine spiral arteries. Here, we utilize 3D imaging, mouse genetics, and pharmacological perturbations to demonstrate that: (1) The mouse placenta invades more extensively than previously recognized with most spiral arteries heavily enveloped by fetal trophoblasts, (2) This process is disrupted without CXCL12-CXCR4 signaling specifically during early pregnancy, and (3) Disrupting early uteroplacental development ultimately results in excessively deep trophoblast invasion, closely mimicking the pregnancy complication placenta accreta. Mechanistically, uterine epithelium, stroma, and arteries activate CXCR4 signaling in early pregnancy, and inhibition causes decidualization failure, followed by dissolution of spiral artery development. Trophoblasts consequently migrate deep into uterine muscle and its arteries, reproducing hallmarks of human accreta. Thus, with 3D imaging, the mouse more effectively models human uteroplacental development and defines an early etiological window for intervention. - Source: PubMed
Publication date: 2026/04/09
Zwierzynski James BMoufarrej Mira NRed-Horse Kristy - Osteoarthritis (OA) is a degenerative joint disease involving multiple cell types, yet the role of osteoblast (OB)-immune cell interactions remains poorly understood. - Source: PubMed
Publication date: 2026/04/11
Liu KunLi Jia-LiChen YanLi Yu-XinDeng Jeffrey DGong YunCao ChongZeng QinXiao Zheng-WuWen Kai-ZhiQu Xiao-ChaoChen Xiang-DingDeng YunDeng Hong-WenTan Li-Jun - Cancer-associated fibroblasts (CAFs) play important roles in breast cancer (BC) progression and metastasis. Here we investigated whether CAFs from indolent vs. aggressive BCs differ in gene expression profiles and how they impact metastasis. - Source: PubMed
Publication date: 2026/04/17
Miller Philip CSharma UtsavTao JiaXiangSun JunMedina-Saenz KelsiePicon-Ruiz ManuelMorata-Tarifa CynthiaBare Susan MSlingerland Joyce MEl-Ashry DorrayaLippman Marc E