Human Polyclonal KRT20 Ab
- Known as:
- Human Polyclonal KRT20 Antibody
- Catalog number:
- a0248
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal KRT20
Related genes to: Human Polyclonal KRT20 Ab
- Gene:
- KRT20 NIH gene
- Name:
- keratin 20
- Previous symbol:
- -
- Synonyms:
- CK20, K20, MGC35423
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-04
- Date modifiied:
- 2016-03-09
Related products to: Human Polyclonal KRT20 Ab
Related articles to: Human Polyclonal KRT20 Ab
- Breast cancer (BC) subtypes such as HR+, HER2+, and triple-negative (TNBC) show distinct molecular features, treatment responses, and outcomes. DNA methylation is a key, targetable epigenetic regulator in BC. This study examined whether the DNA methyltransferase inhibitor decitabine (DAC) produces subtype-specific epigenomic and transcriptional effects in breast cancer cell lines representing distinct molecular subtypes. - Source: PubMed
Publication date: 2026/05/26
Shafqat AreezArora ItikaAkbar ArshiyaAlfuwais MohammedAldubaisi SafiahKhan Mohammad ImranAbu-Zaid AhmedAhmed FirozYaqinuddin Ahmed - Lower urinary tract symptoms (LUTS) represent a spectrum of intractable and progressive disorders. A common pathological feature of LUTS is bladder fibrosis. Here, we established an original mouse model of urinary retention and underactive bladder by ablating urothelial keratin 20. Krt20 deficiency compromised the mechanical load-bearing capacity of umbrella cells, triggering their adaptive expansion and activation of the mechanosensitive protein Yap. Furthermore, loss of Krt20 alters mechanical homeostasis in bladder tissue, stimulating TGF-β/Tgfbr1 signaling activation and subsequently resulting bladder fibrosis. Utilizing this model, we demonstrated a promising therapeutic potential by targeting Tgfbr1-dependent signaling pathway. FFPE snRNA sequencing identified that Alk4/5/7 inhibitor SB-431542 treatment partially rescued the fibrotic bladder microenvironment by attenuating TGF-β signaling derived. Collectively, we present a genetically defined LUTS-fibrosis model and elucidate a mechanotransduction-dependent pathogenic axis, offering innovative avenues for mechanism and therapy exploration. - Source: PubMed
Publication date: 2026/04/27
Jiang JunBao YongjiaHuang TaoZhang HanboMa WensuHe JunweiDuan XianbinMo ChenxiGuo RuiChen JingjieYan FangChen JiehuiLiu XingHuang YichenChen FangChen JiashengDong CongcongGuo Chunming - Chronic kidney disease and its progression to end-stage renal disease represent a major global health burden, driven by renal interstitial fibrosis. The function of the intermediate filament protein Keratin 20 (KRT20) in this context remains largely unexplored. This study investigated the role and mechanism of KRT20 in renal fibrosis. Integrated transcriptomic analysis revealed significant upregulation of KRT20 in fibrotic kidneys. With unilateral ureteral obstruction (UUO) mouse models and TGF-β1-stimulated human renal tubular epithelial (HK-2) cells, we found that KRT20 expression increased progressively with fibrotic severity. Functional studies demonstrated that KRT20 knockdown exacerbated fibrosis and epithelial-mesenchymal transition while its overexpression attenuated. Mechanistically, the transcription factor JUNB, activated by TGF-β1, directly bound to the KRT20 promoter to drive its transcription. Upregulated KRT20 protein subsequently interacted with integrin ITGB1, leading to activation of the PI3K/AKT survival signaling pathway. Collectively, these findings delineated a novel protective “JUNB–KRT20–ITGB1–PI3K/AKT” axis in renal fibrosis, identifying KRT20 as a potential therapeutic target for enhancing endogenous anti-fibrotic response. - Source: PubMed
Publication date: 2026/04/27
Mei HaonanNi XinmiaoZheng QingyuanTang HaoYan ZhiweiYang SongXiong YufengHui YuminJian JunWang JingsongYang XiangxiangLiu XiuhengChen Zhiyuan - Colorectal cancer (CRC) with peritoneal dissemination remains a major therapeutic challenge because of poor prognosis and limited treatment options. Experimental models that accurately recapitulate tumor-mesothelial interactions are scarce. Here, we report the establishment of a novel autologous paired model comprising a CRC cell line (OMUCR-1) and matched cancer-associated mesothelial cells (CAmeso), both simultaneously derived from the malignant ascites of the same patient. Lineage marker analysis using qPCR demonstrated that OMUCR-1 selectively expressed epithelial markers (EPCAM, KRT20), whereas CAmeso strongly expressed mesothelial-mesenchymal markers (ACTA2, MSLN) and lacked epithelial marker expression. These mutually exclusive expression patterns confirm that the two cell populations are phenotypically distinct and rule out cross-contamination. OMUCR-1 displayed strong tumorigenic capacity across multiple transplantation models. CAmeso enhanced CRC cell migration and invasion in vitro, and co-transplantation with OMUCR-1 resulted in larger tumors enriched with αSMA-positive stromal components. RNA sequencing of co-injected xenografts revealed increased expression of murine stromal Fgfr3. Treatment with the FGFR inhibitor BGJ398 reduced tumor growth and decreased stromal FGFR3-positive components, suggesting that stromal FGFR3 may represent a potential microenvironmental vulnerability in CRC with peritoneal dissemination. This autologous CRC-mesothelial system provides a physiologically relevant platform for dissecting tumor-stroma interactions in peritoneal metastasis and may advance stromal-targeted therapeutic strategies. - Source: PubMed
Fukui YasuhiroKasashima HiroakiWang ZizhouOmori IguruKusunoki YukinaEchizen KanaeNonaka YoshikiSeki YukiKuroda KenjiMiki YuichiroYoshii MamiFukuoka TatsunariTamura TatsuroShibutani MasatsuneToyokawa TakahiroMuta YuNakanishi YukiYashiro MasakazuOhtani NaokoMaeda Kiyoshi - BackgroundSignet-ring cell adenocarcinoma of the urinary bladder is a rare and aggressive malignancy. Complete colonic metaplasia of urinary bladder is exceedingly rare, with only 11 patients reported in English literature.PresentationA 56-year-old woman presented with a 6-month history of voiding difficulty and hematuria. She underwent radical cystectomy with hysterectomy, bilateral salpingo-oophorectomy, and pelvic lymph node dissection, and was ultimately diagnosed as primary signet-ring cell adenocarcinoma of the urinary bladder. The entire bladder mucosa, including the ureteric mucosa, showed complete colonic metaplasia. Immunohistochemistry demonstrated a lower gastrointestinal-type immunophenotype, with positivity for KRT20 and CDX2.DiscussionThis report highlights an extremely rare instance of complete colonic metaplasia of the urothelium with subsequent development of signet-ring cell adenocarcinoma. - Source: PubMed
Publication date: 2026/04/10
Mitra SaikatShangloo AksharaBhatkule Milind AAkif Shiraz