Bcl2a1a cDNA ORF clone, Mus musculus(house mouse)

Anti-apoptotic A1 is not essential for lymphoma development in E?-Myc mice but helps sustain transplanted E?-Myc tumour cells.
Mensink M, Anstee NS, Robati M, Schenk RL, Herold MJ, Cory S, Vandenberg CJ
Cell death and differentiation(2018 Jan)

Anti-apoptotic proteins BCL-2, MCL-1 and A1 summate collectively to maintain survival of immune cell populations both in vitro and in vivo.
Carrington EM, Zhan Y, Brady JL, Zhang JG, Sutherland RM, Anstee NS, Schenk RL, Vikstrom IB, Delconte RB, Segal D, Huntington ND, Bouillet P, Tarlinton DM, Huang DC, Strasser A, Cory S, Herold MJ, Lew AM
Cell death and differentiation24(5)878-888(2017 May)

Epstein-Barr virus ensures B cell survival by uniquely modulating apoptosis at early and late times after infection.
Price AM, Dai J, Bazot Q, Patel L, Nikitin PA, Djavadian R, Winter PS, Salinas CA, Barry AP, Wood KC, Johannsen EC, Letai A, Allday MJ, Luftig MA
eLife6(2017 Apr)

Constitutive expression of the anti-apoptotic molecule Bfl1 (A1) in murine vascular Endothelial Cells leads to prolonged allograft survival due to modifying inflammation.
Title: Constitutive expression of the anti-apoptotic Bcl-2 family member A1 in murine endothelial cells leads to transplant tolerance.

Findings identify BCL2A/A1 as a MYC target that can be induced prematurely during B cell development to aid expansion of otherwise cell-death-prone MYC transgenic pre-B cells
Title: MYC selects against reduced BCL2A1/A1 protein expression during B cell lymphomagenesis.

Loss of A1 alone does not impair T cell-driven immune responses. It therefore appears likely that A1 has critical overlapping functions with other pro-survival BCL-2 proteins in T cell immune responses.
Title: The BCL-2 pro-survival protein A1 is dispensable for T cell homeostasis on viral infection.

Conditional knockdown of BCL2A1 reveals rate-limiting roles in BCR-dependent B-cell survival.
Title: Conditional knockdown of BCL2A1 reveals rate-limiting roles in BCR-dependent B-cell survival.

Overexpression of BCL2A1 in T lymphocytes causes selective impairment of TH17 differentiation and protection against autoimmune arthritis.
Title: Selective Impairment of TH17-Differentiation and Protection against Autoimmune Arthritis after Overexpression of BCL2A1 in T Lymphocytes.