CRYAB
- Known as:
- CRYAB
- Catalog number:
- Y213815
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CRYAB
Related genes to: CRYAB
- Gene:
- CRYAB NIH gene
- Name:
- crystallin alpha B
- Previous symbol:
- CRYA2
- Synonyms:
- HSPB5
- Chromosome:
- 11q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1987-09-11
- Date modifiied:
- 2019-04-23
Related products to: CRYAB
Related articles to: CRYAB
- Lumbar spinal stenosis (LSS) caused by hypertrophy of the ligamentum flavum (HLF) is a major cause of lower limb dysfunction; however, its underlying pathogenesis remains unclear. Here we show that metabolic reprogramming and epigenetic modifications synergistically drive HLF progression through a glycolysis-lactylation-fibrosis axis. We demonstrate that HLF tissues exhibit enhanced glycolysis, characterized by elevated extracellular acidification rate, increased ATP production, and upregulated glycolytic enzymes, along with lactate accumulation that positively correlates with tissue thickness. Mass spectrometry identifies CRYAB lysine 92 lactylation (CRYAB_K92la) as a significantly upregulated modification in HLF. Lactylation at CRYAB_K92 promotes fibrosis in human ligamentum flavum cells, whereas the lactylation-blocking mutation CRYAB_K92R attenuates lactate-induced fibrosis and proliferation. Mechanistically, CRYAB_K92 enhances S100A16 transcription, stabilizes S100A16 protein by inhibiting its degradation, and strengthens CRYAB-S100A16 binding, collectively upregulating S100A16 expression. Upregulated S100A16 activates the RAGE signaling pathway, further promoting lactate release and ATP production, thereby forming a positive feedback loop that perpetuates glycolysis, lactate generation, and fibrosis. These findings reveal a novel regulatory axis in HLF pathogenesis and identify CRYAB lactylation, S100A16, and the RAGE pathway as potential therapeutic targets for LSS. - Source: PubMed
Publication date: 2026/05/08
Li JianjunYu ChengCheng JunjieCao YanlinLin TaoNi SongjiaHu KongheDuan Yang - Myocardial fibrosis, a hallmark of heart failure, is driven by pathological crosstalk between stressed cardiomyocytes and activated fibroblasts, yet the initiating signals from cardiomyocytes remain poorly defined. Here, we identify downregulation of casein kinase 2α (CK2α) in cardiomyocytes as a conserved and early trigger of fibrotic remodeling. Cardiomyocyte-specific CK2α loss induces progressive mitochondrial proteome collapse, metabolic reprogramming, and bioenergetic failure. This mitochondrial impairment induces oxidative stress and sterile inflammation, subsequently activating cardiac fibroblasts via paracrine mediators, such as IL-6, thereby establishing a direct mechanistic link between a cardiomyocyte-intrinsic defect and fibroblast activation. Mechanistically, CK2α preserves mitochondrial-cytoskeletal integrity by directly phosphorylating the intermediate filament Desmin at threonine 452 (Thr452). This phosphorylation recruits the chaperone protein αB-crystallin (Cryab) to prevent pathological Desmin aggregation. Disruption of this quality control checkpoint, suffices to recapitulate the full spectrum of mitochondrial dysfunction and pro-fibrotic signaling. Notably, AAV9-mediated restoration of CK2α specifically in cardiomyocytes preserves mitochondrial structure, rescues bioenergetic function, and attenuates fibrosis. Our findings uncover a CK2α-Desmin-mitochondrial quality control axis as a critical metabolic-structural checkpoint in cardiomyocytes and establish that cardiomyocyte-initiated paracrine signaling drives fibroblast activation, highlighting new therapeutic strategies for fibrotic heart disease. - Source: PubMed
Publication date: 2026/05/07
Ma CanjieJia JialiLan JuncongWang JingRao DanRao LanlanZhang WeibinWu DongpengZhang JieWang GangLiu BaohuaAo YingWang Zimei - Gene curation is the analysis of clinical and experimental evidence to determine the strength of relationship between specific genes and diseases. Gene curations allow for improved genetic testing analysis and downstream clinical outcomes. Although variants in crystallin genes are believed to cause about half of all non-syndromic inherited pediatric cataracts, formal gene curations have not been performed. Established and publicly available ClinGen protocols were utilized to perform curations for thirteen crystallin genes to evaluate strength of their associations with pediatric cataracts using published clinical and experimental evidence. Seven genes () scored as Definitively associated with autosomal dominant (AD) inherited pediatric cataracts. Two genes () as Moderate; and four genes have Limited support ( and ). Experimental evidence, when added to clinical evidence, increased the strength of gene-disease relationship for five genes ( from Limited to Definitive, from Moderate to Definitive, CRYGA and from Limited to Moderate and from No Known Disease Relationship (given absence of clinical evidence) to Limited). Optimization and clarification of these gene-disease relationships will improve harmonization of genetic test options (i.e., inclusion on cataract gene panels) and variant interpretation, ultimately allowing for improved clinical care. - Source: PubMed
Publication date: 2026/05/06
Ing AlexanderWeisman Allison GoetschDrackley AndyMcMullen PatrickSkol AndrewLewis FrankEvans BradyYap Kai LeeRathbun PamelaGordon AdamRalay Ranaivo HantaBohnsack Brenda LRossen Jennifer Landau - Desmin cardiomyopathy is a rare hereditary cardiomyopathy caused by DES gene variants, often presenting with a spectrum of phenotypes and frequently associated with a poor prognosis. - Source: PubMed
Publication date: 2026/04/30
Yu MengdiPu LutongWang JieChen Yucheng - This study investigates the molecular mechanism by which SPI1 inhibits ferroptosis and immune escape in bladder cancer (BC) through upregulation of CRYAB expression. Bioinformatics was utilized to screen BC-related prognostic genes and their upstream regulators. RT-qPCR and Western blot (WB) were conducted to assess SPI1 and CRYAB expression in BC cells. CRYAB knockdown and SPI1/CRYAB overexpression were performed to explore their effects on cellular behaviors. Malignant phenotypes were evaluated through CCK-8, colony formation, scratch assays, and Annexin V-FITC/PI staining. Ferroptosis was assessed using Fe²⁺ and JC-1 staining, alongside biochemical analysis. THP-1 monocytes were differentiated into macrophages and co-cultured with BC cells; WB was performed to measure M2 macrophage polarization markers (CD86/CD206). T cell cytotoxicity assays were performed using activated CD3 T cells from healthy donors co-cultured with BC cells to directly assess immune evasion. Dual-luciferase and ChIP-qPCR assays were used to explore the transcriptional regulation of CRYAB by SPI1. A xenograft mouse model was established to examine BC cell growth and immune escape in vivo. Bioinformatics identified CRYAB and SPI1 as key regulators in BC. Both were highly expressed in BC cells. CRYAB knockdown promoted ferroptosis and inhibited malignant behaviors of BC cells, and suppressed epithelial-mesenchymal transition (EMT) and M2 macrophage polarization in co-culture systems. Furthermore, CRYAB or SPI1 knockdown sensitized BC cells to T cell-mediated killing and enhanced T cell effector molecule production (IFN-γ, TNF-α, Granzyme B), whereas CRYAB overexpression reversed the effect of SPI1 knockdown. Dual-luciferase and ChIP-qPCR assays confirmed that SPI1 directly transcriptionally regulates CRYAB. SPI1 knockdown enhanced ferroptosis, inhibited EMT, and suppressed immune escape in BC cells, effects that were reversed by CRYAB overexpression. SPI1 inhibits ferroptosis and immune escape in BC by promoting CRYAB expression, thereby facilitating BC progression. These findings provide new theoretical insights and potential therapeutic strategies to improve the prognosis of BC patients. - Source: PubMed
Publication date: 2026/04/22
Chen HaoYang GuanglinWei LiweiCui ZelinZhao QiyueMo QizhouWen JianhuaYang ShuboYu JiayinHuang YichenTan ShutingQin MinCheng Jiwen