Disease relevance of JUNB

• Twenty-four percent of cases, including 7 of 10 cases of primary cutaneous CD30(+) anaplastic large-cell lymphoma (C-ALCL), 4 of 14 MF, 4 of 22 SS, and 2 of 23 primary cutaneous B-cell lymphoma (PCBCL) showed amplification of JUNB, and high-level amplification of this oncogene was present in 3 C-ALCL and 2 MF cases [1].
• Amplification and overexpression of JUNB is associated with primary cutaneous T-cell lymphomas [1].
• These included transcripts encoding acute phase response proteins, IER2 and JUNB, and regulators of cell proliferation, p21Cip1 and KLF6 [2].
• PU.1 and Junb: Suppressing the formation of acute myeloid leukemia stem cells [3].
• In the comparison between the affected and unaffected psoriatic skin, the transcription factor JUNB was found at the top of the statistical rankings for the up-regulated genes in affected skin, suggesting that it has an important but as yet undefined role in psoriasis [4].

High impact information on JUNB

• Phorbol ester-induced amino-terminal phosphorylation of human JUN but not JUNB regulates transcriptional activation [5].
• Amplification of JUNB was studied in 104 DNA samples from 78 PCL cases using real-time polymerase chain reaction [1].
• Furthermore, we observed an uncoupling of EGR1, JUNB, and WNT signaling in response to SS18-SSX2 expression, suggesting that the SWI/SNF-associated coactivation functions of the SS18 moiety are impaired [6].
• The latter display the highest DNA binding affinity for the TGF-beta-response elements of JUNB and collagen 7 [7].
• Transcription factor jun-B is target of autoreactive T-cells in IDDM [8].

Biological context of JUNB

• Thus, we propose that phorbol esters enhance the trans-activation potential of JUN, but not JUNB, by the phosphorylation of the N-terminal regulatory domain of JUN [5].
• In contrast, TGF-beta down-regulates collagenase gene expression through the induction of the jun-B proto-oncogene [9].
• Prkcl1 maps to mouse chromosome 8 between D8Mit6 and junb [10].

Anatomical context of JUNB

• Increased expression of JUNB was also identified in the MF cell line [11].

Regulatory relationships of JUNB

• By using DNA-array techniques and Northern blot analysis, we here revealed that TFPI transiently induced the mRNA expression of JUNB and GADD45B [12].

Other interactions of JUNB

• Immunohistochemical staining of paraffin sections from six cases demonstrated expression of JUNB protein in five cases and BCL2 in three cases [13].
• This region was found to be sufficient for the phorbol ester-inducible transcriptional activity of JUN, but not JUNB [5].
• Tissue factor pathway inhibitor induces expression of JUNB and GADD45B mRNAs [12].
• TPA but not AII increased the level of the transcription factor JunB in nuclear extracts and the increase was partially abolished by the MEK1 inhibitor PD98059 [14].

References