Nabp1, also known as hSSB2 and OBFC2A, is a single-stranded nucleic-acid-binding protein. It contains an OB motif at its N-terminus. Nabp1 is involved in multiple biological processes. It plays a role in the cellular response to DNA UV damage, where it is required for the recruitment of RPA, and is also related to nucleotide excision repair pathway [1]. It is regulated by RORgamma2 during thymopoiesis and localizes to the nucleus as part of a high-molecular-mass protein complex [2].

Ssb2/Nabp1 knockout mice show that Nabp1 is dispensable for thymic maturation, male fertility, and DNA repair in mice. There are no marked phenotypic changes in Ssb2(-/-) mice compared to their littermates, and Ssb1 may compensate for the loss of Ssb2 in these aspects [4]. In HBV-related HCC after TACE, increased NABP1+ malignant hepatocytes are related to poor TACE response and dismal prognosis, and knockdown of NABP1 significantly inhibits the proliferation and migration of HCC cells in vitro [3]. In cisplatin-induced acute kidney injury, ZC3H13 promotes the m6A modification of NABP1, enhancing its mRNA stability, and inhibition of ZC3H13 alleviates G2/M arrest, apoptosis, and kidney injury by affecting NABP1 expression [5].

In conclusion, Nabp1 is important in DNA damage response and has implications in certain disease conditions such as HBV-related HCC and acute kidney injury. The gene knockout mouse models have revealed that Nabp1 is not essential for thymic maturation, male fertility, and DNA repair in mice, while also highlighting its potential role in cancer progression and kidney injury, providing insights into disease mechanisms and potential therapeutic targets.