|
Functions of Jun and Fos proteins |
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| Activator protein 1 protein |
Phenotype |
Affected organs/cells |
|
|
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| Transgenic |
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| H2Kb-Jun |
None |
None |
| Ubiquitin C-JunBa |
Increased bone mass |
Not defined |
| CD4-JunB |
Enhanced T helper cell 2 maturation |
Thymus, CD4 thymocytes |
| Ubiquitin C-JunD |
Peripheral T cells and B cells reduced |
Lymphocytes |
| H2Kb-Fos |
Osteosarcoma |
Bone, osteoblasts |
| H2Kb-Fos/Rsk-2-/y |
Reduced osteosarcoma |
Bone, osteoblasts |
| H2Kb-FosB |
None |
Bone |
| TCRβ-ΔFosB |
Impaired T cell differentiation |
Thymus, immature thymocytes |
| NSE-ΔFosB |
Osteosclerosis |
Bone, osteoblasts |
| H2Kb-Fra-1 |
Osteosclerosis |
Bone, osteoblasts |
| CMV-Fra-2 |
Occular malformations |
Anterior eye structure |
| H2Kb-Fra-2a |
Increased bone mass, fibrosis |
Bone, internal organs, skin |
| Knockout |
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| Jun |
Embryonic lethal on embryonic day 12.5 |
Liver, heart, neural crest |
| JunB |
Embryonic lethal on embryonic day 10 |
Extraembryonic tissues |
| JunD |
Male sterility |
Testis, spermatides |
| c-Fos |
Osteopetrosis |
Bone, osteoclasts |
| FosB |
Nurturing defect |
Brain, hypothalamus |
| Fra-1 |
Embryonic lethal on embryonic day 9.5 |
Extraembyonic tissue |
| Fra-2 |
Lethal at birth |
Bone, osteoclasts |
| Conditional |
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| Alfp-cre Jun |
Liver regeneration defect |
Liver, hepatocytes |
| Col2a1-cre Jun |
Scoliosis |
Bone, notochordal cells |
| Nestin-cre Jun |
Axonal regeneration defect |
Central nervous system, motoneurons |
| MORE-cre JunB |
Osteopenia |
Bone, osteoclasts, osteoblasts |
| K5-cre Jun |
Eyes open at birth, reduced skin tumors |
Keratinocytes |
| Nestin-cre Fos |
Learning defects |
Brain, hippocampal neurons |
| MORE-cre Fra-1 |
Osteopenia |
Bone, osteoblasts |
| Inducible |
||
| K5-creERTJunB + Jun |
Psoriasis-like disease |
Skin, joints, keratinocytes |
|
Knockout, conditional knockout and gain of function (transgenic) approaches applied to study the role of Jun and Fos proteins during development and in diseases. The gain-of-function approaches were performed with different promoters, either leading to ubiquitous expression (for example, H2Kb, ubiquitin C, or cytomegalovirus (CMV)) or to tissue-specific expression (for example, CD4, TCRβ, or neuron-specific enolase (NSE)) of the transgenes. aUnpublished data from the Wagner Laboratory. | ||
Zenz et al. Arthritis Research & Therapy 2008 10:201 doi:10.1186/ar2338 |
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