Acvr1b-KO Mouse

Acvr1b, also known as activin A receptor type 1B or ALK4, is a member of the transforming growth factor-β (TGF-β) superfamily. It mediates the signaling of several TGF-β superfamily ligands and is involved in various biological processes such as cell proliferation, apoptosis, and differentiation. Genetic models, like knockout (KO) and conditional knockout (CKO) mouse models, have been crucial for studying its functions [1,2,3,4,5].

In pancreatic cancer research, Acvr1b loss in mice with Kras mutations in acinar or ductal cells increased the formation of pancreatic intraepithelial neoplasia and IPMN-like lesions, indicating its role in pancreatic precancerous lesion development [1]. In skeletal muscle, combined muscle-specific KO of Tgfbr1 and Acvr1b in mice induced myofibre hypertrophy and accelerated muscle regeneration, showing their synergistic involvement in muscle-related processes [4]. Conditional Acvr1b knockout (Acvr1b(flox/flox); K14-Cre) mice had hair loss abnormalities due to disrupted hair follicle cycling and development, demonstrating a specialized role for Acvr1b in hair-related biology [5].

In conclusion, Acvr1b plays essential roles in multiple biological processes. Studies using KO and CKO mouse models have revealed its significance in pancreatic precancerous lesion formation, muscle function, and hair follicle development. These findings contribute to understanding the molecular mechanisms underlying related diseases and biological functions, potentially providing new insights for disease prevention and treatment [1,4,5].

References:

1. Saeki, Kiyoshi, Wood, Ian S, Wang, Wei Chuan Kevin, Su, Gloria H, Kopp, Janel L. 2024. Acvr1b Loss Increases Formation of Pancreatic Precancerous Lesions From Acinar and Ductal Cells of Origin. In Cellular and molecular gastroenterology and hepatology, 18, 101387. doi:10.1016/j.jcmgh.2024.101387. https://pubmed.ncbi.nlm.nih.gov/39111635/

2. Preechanukul, Anucha, Yimthin, Thatcha, Tandhavanant, Sarunporn, Chantratita, Narisara, Garand, Mathieu. 2023. Abundance of ACVR1B transcript is elevated during septic conditions: Perspectives obtained from a hands-on reductionist investigation. In Frontiers in immunology, 14, 1072732. doi:10.3389/fimmu.2023.1072732. https://pubmed.ncbi.nlm.nih.gov/37020544/

3. Akimoto, Yuki, Fujii, Wataru, Naito, Kunihiko, Sugiura, Koji. 2023. The effect of ACVR1B/TGFBR1/ACVR1C signaling inhibition on oocyte and granulosa cell development during in vitro growth culture. In The Journal of reproduction and development, 69, 270-278. doi:10.1262/jrd.2023-041. https://pubmed.ncbi.nlm.nih.gov/37722883/

4. Hillege, Michèle M G, Shi, Andi, Galli, Ricardo A, Hoogaars, Willem M H, Jaspers, Richard T. 2022. Lack of Tgfbr1 and Acvr1b synergistically stimulates myofibre hypertrophy and accelerates muscle regeneration. In eLife, 11, . doi:10.7554/eLife.77610. https://pubmed.ncbi.nlm.nih.gov/35323108/

5. Qiu, Wanglong, Li, Xiaojun, Tang, Hongyan, Owens, David M, Su, Gloria H. 2010. Conditional activin receptor type 1B (Acvr1b) knockout mice reveal hair loss abnormality. In The Journal of investigative dermatology, 131, 1067-76. doi:10.1038/jid.2010.400. https://pubmed.ncbi.nlm.nih.gov/21191412/