{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n GALNT11 is a member of the widely conserved UDP‐N‐acetylgalactosamine:polypeptide N‐acetylgalactosaminyltransferase family that initiates mucin‐type O‐glycosylation by transferring GalNAc from UDP–GalNAc to serine and threonine residues on target proteins. Functional studies indicate that GALNT11 can play multifaceted roles in modulating protein glycosylation and, consequently, cell signaling and function. For example, GALNT11 is implicated in the glycosylation of linker regions on receptors such as the low‐density lipoprotein receptor, suggesting that it participates in ensuring proper receptor stability and function through O‐glycan modification (see."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In addition, genetic evidence from genome‐wide association studies has linked polymorphisms in GALNT11 with the rapid decline of kidney function, pointing to a potential role in renal pathophysiology."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " GALNT11 has also been shown to be a determinant in opioid‐induced respiratory depression, where its enzymatic activity appears to govern glycosylation events that modulate the sensitivity of respiratory regulatory pathways."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n In the context of cancer, aberrant expression of GALNT11 has been observed. In chronic lymphocytic leukemia (CLL), for instance, marked over‐expression of GALNT11 distinguishes malignant B‐cells from their normal counterparts and may serve as a molecular marker of disease prognosis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": " Similarly, copy number variations involving GALNT11 have been associated with colorectal cancer susceptibility, suggesting that gene dosage effects may influence tumor development"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": ", and triplication of the genomic region containing GALNT11 is proposed to affect Notch signaling through altered O‐glycosylation, thereby contributing to congenital malformations."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Finally, pharmacologic studies in cancer models reveal that a reduction in GALNT11 levels can correlate with decreased multidrug resistance and altered cell survival. In breast cancer cell models subjected to photodynamic treatment—as well as in studies of colon cancer stem cells undergoing endothelial trans‐differentiation—lower GALNT11 levels were associated with increased apoptosis and reduced drug transporter activity, underscoring a potential role for GALNT11 in modulating treatment response."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these findings suggest that GALNT11, through its catalytic control of O‐glycosylation, contributes to the regulation of receptor function, influences key signaling pathways such as Notch, and impacts diverse biological processes ranging from renal function and respiratory control to cancer progression and chemotherapeutic sensitivity."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}, {"type": "fg_fs", "start_ref": "5", "end_ref": "8"}]}, {"type": "t", "text": "\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Nis Borbye Pedersen, Shengjun Wang, Yoshiki Narimatsu, et al. 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