KIAA1199 Blocking Peptide
- Known as:
- KIAA1199 Blocking Peptide
- Catalog number:
- 33r-7080
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- KIAA1199 Blocking Peptide
Related genes to: KIAA1199 Blocking Peptide
- Gene:
- CEMIP NIH gene
- Name:
- cell migration inducing hyaluronidase 1
- Previous symbol:
- KIAA1199
- Synonyms:
- IR2155535, TMEM2L, HYBID
- Chromosome:
- 15q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-29
- Date modifiied:
- 2018-02-26
Related products to: KIAA1199 Blocking Peptide
Related articles to: KIAA1199 Blocking Peptide
- Vocal fold scarring (VFS) is a debilitating fibrotic disorder lacking molecular biomarkers for early detection or for monitoring toxicant-induced injury. Cigarette smoke toxicity (CST), a major environmental driver of vocal fold fibrosis, disrupts extracellular matrix (ECM) homeostasis; however, the mechanisms linking CST to fibrotic remodeling remain poorly understood. Here, we identify CD44, a hyaluronan receptor, as a key regulator of CST-induced VFS and healthy human vocal fold fibroblast (hVFF) homeostasis. CD44 depletion reduced elastin, collagen, and lysyl oxidase mRNA expression and increased conditioned medium viscosity, demonstrating its essential role in maintaining ECM composition and viscoelastic properties. Cigarette smoke extract (CSE; 2.5-20%) induced concentration-dependent morphological alterations and cytotoxicity in hVFFs. At the median lethal concentration (LC₅₀, 5% CSE), exposure increased collagen synthesis, Na⁺/H⁺ exchanger (NHE1) expression, oxidative stress, and p53-mediated apoptosis. CSE promoted degradation of high-molecular-weight hyaluronan (500-1100 kDa) into low-molecular-weight fragments (30.6-550 kDa) within the ECM via CD44 and hyaluronidase but not through CEMIP, leading to glycocalyx disruption, impaired wound repair and profibrotic remodeling. These findings identify the CD44-dependent hyaluronan-catabolic pathway as a central mediator of CST-induced ECM remodeling. CD44 exhibited a context-dependent dual role in hVFF responses to CSE, acting protectively during short-term exposure (5%, 24 h) but promoting detrimental cellular responses with increasing CSE concentration (≥5%) and prolonged exposure (≥72 h). A synergistic pair of small-molecule inhibitors targeting CD44 signaling and structural integrity reduced oxidative stress, normalized intracellular pH, maintained hyaluronan homeostasis, suppressed p53 expression, restored CD44 expression, attenuated inflammation, and improved wound healing. Collectively, these findings identify CD44 as a promising molecular indicator of early VFS-associated changes and a potential therapeutic target for CST-induced profibrotic remodeling. - Source: PubMed
Publication date: 2026/08/06
Basu KaustuvMongeau Luc - Colorectal cancer (CRC) is a leading cause of cancer death worldwide, mainly due to cancer cell proliferation and migration. Although chondroitin sulfate (CS) is involved in cancer progression, its regulatory mechanisms remain unclear. - Source: PubMed
Publication date: 2026/06/29
Ye YingyiLiang YihaoLan HuanZhang NanKe YujingAn LinLiu ZhongqiuWang Caiyan - Fascia, the connective tissue network enveloping muscles, organs, and viscera, functions as a hyaluronan (HA)-rich adaptive interface that senses and responds to inflammatory cues. This narrative review synthesizes ECM literature across niches to examine the calcium-hyaluronan (CHA) axis, a feedback loop linking Ca² signaling to HA synthesis via HAS2 and molecular weight-dependent signaling through CD44 and RHAMM receptors. We propose that the CHA axis is constrained further by ATP/NAD-mediated feedback and functions as a rheostat regulated by four distinct constraint types (1): Mechanical loading and shear regulate HA turnover, hydration, and viscosity via YAP/TAZ and integrin mechanosensing (2). Inflammatory cytokines drive HAS2/HA accumulation during chronic irritation or injury through CD44/RHAMM signaling (3). Metabolic energy availability provides purinergic brakes via AMPK/SIRT1 that suppress synthesis when ATP is scarce (4). HA clearance mechanisms-hyaluronidases, TMEM2/CEMIP, lymphatic drainage, and interstitial fluid flow-which may be as critical as synthesis itself. This is the first review integrating the domains of research across cell types, with clinical relevance in cancer and wound healing as well as exercise physiology and longevity protocols. - Source: PubMed
Publication date: 2026/06/17
Kirkness Karen Bda Silva Fabiana CSchleip RobertCruvinel-Júnior Ronaldo HScarlata Suzanne - It is documented that antigens can induce immune responses able to regulate complex diseases. Conversely, the dysregulated inflammatory response in leprosy increases morbidity and leads to reactional episodes, impairing the disease pathogenesis. The goal of this study was to evaluate the potential of the (Sm29) antigen in regulating the immune response in leprosy through a transcriptome study across clinical reactional forms: reversal reaction (RR), and erythema nodosum leprosum (ENL), and without reaction (WR). - Source: PubMed
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