Junb cDNA ORF clone, Mus musculus(house mouse)

AP-1 Transcription Factors and the BAF Complex Mediate Signal-Dependent Enhancer Selection.
Vierbuchen T, Ling E, Cowley CJ, Couch CH, Wang X, Harmin DA, Roberts CWM, Greenberg ME
Molecular cell68(6)1067-1082.e12(2017 Dec)

Data show that JunB is a nonredundant regulator of transcriptional programs that support Th17 cell identity and restrain alternative Th1 and Treg cell fates.
Title: JunB promotes Th17 cell identity and restrains alternative CD4

the present data demonstrates for the first time that JunB plays an important role in the formation of embryonic vascular networks.
Title: JunB regulates angiogenesis and neurovascular parallel alignment in mouse embryonic skin.

BATF/JUN-B and BATF/C-JUN complexes play important roles in OA cartilage destruction through regulating anabolic and catabolic gene expression in chondrocytes.
Title: Inhibition of BATF/JUN transcriptional activity protects against osteoarthritic cartilage destruction.

Study shows that myeloid deletion of JUNB dampens immune polarization and reshapes disease outcomes during infection with both P. berghei and N. brasiliensis by limiting type 1 and type 2 responses, respectively. Thus, JUNB is an important regulator of myeloid responses to both type 1 and type 2 infections in vivo.
Title: Myeloid expression of the AP-1 transcription factor JUNB modulates outcomes of type 1 and type 2 parasitic infections.

JunB and c-Jun expression in post-mitotic oligodendrocytes is mostly dispensable for the maintainance of white matter tracts throughout adult life, even under demyelinating conditions.
Title: Deletion of Jun proteins in adult oligodendrocytes does not perturb cell survival, or myelin maintenance in vivo.