The APOBEC family of proteins perform mRNA modifications by deaminating cytidine bases to uracil. The N-terminal domain of APOBEC-like proteins is the catalytic domain, while the C-terminal domain is a pseudocatalytic domain. More specifically, the catalytic domain is a zinc dependent cytidine deaminase domain and is essential for cytidine ...

在 apobec 家族中，apobec3b 是各种癌症中研究最广泛的成员。 对apobec研究的意义; apobec(载脂蛋白b mrna编辑酶)家族介导的诱变在人类癌症中广泛存在。然而，现在对apobecs和apobec突变在癌症中的生物学特征和临床相关性的了解仍然有限。 二、研究结果

载脂蛋白 B mRNA 编辑酶催化多肽 (apolioprotein B mRNA-editing enzyme catalytic polypeptide, APOBEC) 家族是一类高效的胞苷脱氨酶，能够特异催化基因组中的胞嘧啶变为尿嘧啶（C>U），其转录可被促炎症细胞因子和趋化因子激活，并在人体的固有和获得性免疫机制中发挥 …

The APOBEC (Apolipoprotein B mRNA Editing Catalytic Polypeptide-like) family of proteins has diverse and important functions in human health and disease. These proteins have an intrinsic ability to bind to both RNA and single-stranded (ss)DNA.

The APOBEC (apolipoprotein B mRNA editing catalytic polypeptide-like) family of proteins have diverse and important functions in human health and disease. These proteins have an intrinsic ability to bind to both RNA and single-stranded (ss) DNA. Both function and tissue-specific expression varies widely for each APOBEC protein.

2023年7月8日 · apobec突变信号在靶向治疗延长反应后进展的肺癌患者的肿瘤中富集。 本研究表明，在预防或延迟获得性耐药的肺癌靶向治疗中，诱导A3A对靶向治疗的反应驱动耐药细胞的进化，这表明抑制A3A的表达或活性可能是一种潜在的治疗策略。

apobec（“载脂蛋白质b mrna编辑催化多肽”）是一类进化保守的胞苷脱氨酶家族。 在人体内，已知含有保守的DNA胞嘧啶脱氨酶结构域的基因共有11种，包括AID、APOBEC1、APOBEC2、APOBEC3基因家族APOBEC3A、APOBEC3B、APOBEC3C、APOBEC3DE、APOBEC3F、APOBEC3G、APOBEC3H（分别称为A3A、A3B ...

apobec("载脂蛋白质b mrna编辑催化多肽")是一类进化保守的胞苷脱氨酶家族。...

2017年9月20日 · In urothelial carcinomas, APOBEC-mediated mutagenesis is enriched in chemotherapy-treated carcinomas and the TpC mutational signature has been found in some chemotherapy-resistant pathways, e.g., ATP-binding cassette transporter family proteins and homologous recombination repair proteins.

2017年9月20日 · Here, we review the physiological functions and structural characteristics of APOBEC family members and their roles as endogenous mutators that contribute to hypermutations during carcinogenesis. We also review the various iterations of the APOBEC-CRISPR/Cas9 gene-editing tools, pointing out their features and limitations as well as the ...