c-jun gene、c-Jun protein

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the 3rd letter of the Roman alphabet (同)c
(music) the keynote of the scale of C major
a general-purpose programing language closely associated with the UNIX operating system

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/11/21 05:41:57」(JST)

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c-Jun is a protein that in humans is encoded by the JUN gene. c-Jun in combination with c-Fos, forms the AP-1 early response transcription factor. It was first identified as the Fos-binding protein p39 and only later rediscovered as the product of the c-jun gene. It is activated through double phosphorylation by the JNK pathway but has also a phosphorylation-independent function. c-jun knockout is lethal, but transgenic animals with a mutated c-jun that cannot be phosphorylated (termed c-junAA) can survive.

This gene is the putative transforming gene of avian sarcoma virus 17. It encodes a protein that is highly similar to the viral protein, and that interacts directly with specific target DNA sequences to regulate gene expression. This gene is intronless and is mapped to 1p32-p31, a chromosomal region involved in both translocations and deletions in human malignancies.^[3]

1 Function
- 1.1 Regulation
- 1.2 Cell cycle progression
- 1.3 Anti-apoptotic activity
2 Clinical significance
- 2.1 Cancer
- 2.2 Tumor initiation
- 2.3 Breast cancer
- 2.4 Cellular differentiation
3 As anti-cancer drug target
4 Anti-cancer property of c-jun
- 4.1 p16INK4a
- 4.2 Tylophorine
5 Interactions
6 See also
7 References
8 Further reading
9 External links

Function

Regulation

Both Jun and its dimerization partners in AP-1 formation are subject to regulation by diverse extracellular stimuli, which include peptide growth factors, pro-inflammatory cytokines, oxidative and other forms of cellular stress, and UV irradiation. For example, UV irradiation is a potent inducer for elevated c-jun expression.^[4]

The c-jun transcription is autoregulated by its own product, Jun. The binding of Jun (AP-1) to a high-affinity AP-1 binding site in the jun promoter region induces jun transcription. This positive autoregulation by stimulating its own transcription may be a mechanism for prolonging the signals from extracellular stimuli. This mechanism can have biological significance for the activity of c-jun in cancer.^[5]

Also, the c-jun activity can be regulated by the ERK pathway. Constitutively active ERK is found to increase c-jun transcription and stability through CREB and GSK3. This results in activated c-jun and its downstream targets such as RACK1 and cyclin D1. RACK1 can enhance JNK activity, and activated JNK signaling subsequently exerts regulation on c-jun activity.^[6]

Phosphorylation of Jun at serines 63 and 73 and threonine 91 and 93 increases transcription of the c-jun target genes.^[7] Therefore, regulation of c-jun activity can be achieved through N-terminal phosphorylation by the Jun N-terminal kinases (JNKs). It is shown that Jun’s activity (AP-1 activity) in stress-induced apoptosis and cellular proliferation is regulated by its N-terminal phosphorylation.^[8] Another study showed that oncogenic transformation by ras and fos also requires Jun N-terminal phosphorylation at Serine 63 and 73.^[9]

Cell cycle progression

Studies show that c-jun is required for progression through the G1 phase of the cell cycle, and c-jun null cells show increased G1 arrest. C-jun regulates the transcriptional level of cyclin D1, which is a major Rb kinase. Rb is a growth suppressor, and it is inactivated by phosphorylation. Therefore, c-jun is required for maintaining sufficient cyclin D1 kinase activity and allowing cell cycle progression.^[4]

In cells absent of c-jun, the expression of p53 (cell cycle arrest inducer) and p21 (CDK inhibitor and p53 target gene) is increased, and those cells exhibit cell cycle defect. Overexpression of c-jun in cells results in decreased level of p53 and p21, and exhibits accelerated cell proliferation. C-jun represses p53 transcription by binding to a variant AP-1 site in the p53 promoter. Those results indicate that c-jun downregulates p53 to control cell cycle progression.^[10]

Anti-apoptotic activity

UV irradiation can activate c-jun expression and the JNK signaling pathway. C-jun protects cells from UV-induced apoptosis, and it cooperates with NF-κB to prevent apoptosis induced by TNFα. The protection from apoptosis by c-jun requires serines 63/73 (involved in phosphorylation of Jun), which is not required in c-jun-mediated G1 progress. This suggests that c-jun regulates cell cycle progression and apoptosis through two separated mechanisms.^[4]

A study utilized liver-specific inactivation of c-jun in hepatocellular carcinoma, which showed impaired tumor development correlated with increased level of p53 protein and the mRNA level of the p53 target gene noxa. Also, c-jun can protect hepatocytes from apoptosis, as hepatocytes lacking c-jun showed increased sensitivity to TNFα-induced apoptosis. In those hepatocytes lacking c-jun, deletion of p53 can restore resistance toward TNFα. Those results indicate that c-jun antagonizes the proapoptotic activity of p53 in liver tumor.^[11]

Clinical significance

It is known that c-jun plays a role in cellular proliferation and apoptosis of the endometrium throughout the menstrual cycle. The cyclic change of the c-jun protein levels is significant in the proliferation and apoptosis of glandular epithelial cells. The persistent stromal expression of c-jun protein may prevent stromal cells from entering into apoptosis during the late secretory phase.^[12]

Cancer

C-jun is a proto-oncogene (its protein is Jun) and is the cellular homolog of the viral oncoprotein v-jun.^[4] Jun is the first discovered oncogenic transcription factor.^[13]

In a study using non-small cell lung cancers (NSCLC), c-jun was found to be overexpressed in 31% of the cases in primary and metastatic lung tumors, whereas normal conducting airway and alveolar epithelia in general did not express c-jun.^[14]

A study with a group consisted of 103 cases of phase I/II invasive breast cancers showed that activated c-jun is expressed predominantly at the invasive front of breast cancer and is associated with proliferation and angiogenesis.^[15]

Tumor initiation

A study was done with liver-specific inactivation of c-jun at different stages of tumor development in mice with chemically induced hepatocellular carcinomas. The result indicates that c-jun is required at the early stage of tumor development, and deletion of c-jun can largely suppress tumor formation. Also, c-jun is required for tumor cell survival between the initiation and progression stages. In contrast to that, inactivation of c-jun in advanced tumors does not impair tumor progression.^[11]

Breast cancer

Overexpression of c-jun in MCF-7 cells can result in overall increased aggressiveness, as shown by increased cellular motility, increased expression of a matrix-degrading enzyme MMP-9, increased in vitro chemoinvasion, and tumor formation in nude mice in the absence of exogenous estrogens. The MCF-7 cells with c-jun overexpression became unresponsive to estrogen and tamoxifen, thus c-jun overexpression is proposed to lead to an estrogen-independent phenotype in breast cancer cells. The observed phenotype for MCF-7 cells with c-jun overexpression is similar to that observed clinically in advanced breast cancer, which had become hormone unresponsive.^[16]

The invasive phenotype contributed by c-jun overexpression is confirmed in another study. In addition, this study showed increased in vivo liver metastasis by the breast cancer with c-jun overexpression. This finding suggests that c-jun plays a critical role in the metastasis of breast cancer.^[17]

In mammary tumors, endogenous c-jun was found to play a key role in ErbB2-induced migration and invasion of mammary epithelial cells. Jun transcriptionally activates the promoters of SCF (stem cell factor) and CCL5. The induced SCF and CCL5 expression promotes a self-renewing mammary epithelial population. It suggests that c-jun mediates the expansion of breast cancer stem cells to enhance tumor invasiveness.^[18]

Cellular differentiation

Ten undifferentiated and highly aggressive sarcomas showed amplification of the jun gene and JUN overexpression at both RNA and protein levels. Overexpression of c-jun in 3T3-L1 cells (a preadipocytic non-tumoral cell line that resembles human liposarcoma) can block or delay adipocytic differentiation of those cells.^[19]

As anti-cancer drug target

A study showed that oncogenic transformation by ras and fos requires Jun N-terminal phosphorylation at Serine 63 and 73 by the Jun N- terminal kinases (JNK). In this study, the induced skin tumor and osteosarcoma showed impaired development in mice with a mutant Jun incapable of N-terminal phosphorylation.^[9] Also, in a mouse model of intestinal cancer, genetic abrogation of Jun N-terminal phosphorylation or gut-specific c-jun inactivation attenuated cancer development and prolonged lifespan.^[7] Therefore, targeting the N-terminal phosphorylation of Jun (or the JNK signaling pathway) can be a potential strategy for inhibiting tumor growth.

In melanoma-derived B16-F10 cancer cells, c-jun inactivation by a pharmacological JNK/jun inhibitor SP combined with JunB knockdown can result in cytotoxic effect, leading to cell arrest and apoptosis. This anti-JunB /Jun strategy can increase the survival of mice inoculated with tumor cells, which suggests a potential antitumor strategy through Jun and JunB inhibition.^[20]

Anti-cancer property of c-jun

Most research results show that c-jun contributes to tumor initiation and increased invasiveness. However, a few studies discovered some alternative activities of c-jun, suggesting that c-jun may actually be a double-edge sword in cancer.

p16INK4a

p16INK4a is a tumor suppressor and a cell cycle inhibitor, and a study shows that c-jun acts as “bodyguard” to p16INK4a by preventing methylation of the p16INK4a promoter. Therefore, c-jun can prevent silencing of the gene p16INK4a.^[21]

Tylophorine

Tylophorine is a type of plant-derived alkaloid with anticancer activity by inducing cell cycle arrest. A study demonstrated that tylophorine treatment increased c-jun protein accumulation. Then c-jun expression in conjunction with tylophorine promotes G1 arrest in carcinoma cells through the downregulation of cyclin A2. Therefore, the result indicates that the anticancer mechanism of tylophorine is mediated through c-jun.^[22]

Interactions

C-jun has been shown to interact with:

ATF2^[23]^[24]^[25]
AR^[26]
ASCC3^[27]
ATF3^[25]^[28]^[29]
BCL3^[30]
BCL6^[31]
BRCA1^[32]
C-Fos^[33]^[34]^[35]^[36]^[37]^[38]^[39]
CSNK2A1^[40]
NELFB^[41]
COPS5^[42]
CREBBP^[43]
CSNK2A2^[40]
DDX21,^[44]
DDIT3^[45]
ERG^[46]
ETS2,^[47]
FOSL1^[34]
TGIF1^[48]
MAPK8^[49]^[50]^[51]^[52]^[53]^[54]^[55]^[56]
SMAD3^[57]^[58]^[59]
MyoD^[60]
NACA^[61]
NFE2L1^[39]
NFE2L2^[39]
NCOR2^[62]
NCOA1^[63]^[64]^[65]
PIN1^[66]
RBM39^[67]
RELA^[36]
RB1^[68]
RFWD2^[69]^[70]
RUNX1^[71]^[72]
RUNX2^[71]^[72]
STAT1^[73]
STAT3^[73]
TBP^[74] and
GTF2B.^[74]

References

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^ Lee SK, Kim JH, Lee YC, Cheong J, Lee JW (2000). "Silencing mediator of retinoic acid and thyroid hormone receptors, as a novel transcriptional corepressor molecule of activating protein-1, nuclear factor-kappaB, and serum response factor". The Journal of Biological Chemistry. 275 (17): 12470–4. doi:10.1074/jbc.275.17.12470. PMID 10777532.
^ Lee SK, Anzick SL, Choi JE, Bubendorf L, Guan XY, Jung YK, Kallioniemi OP, Kononen J, Trent JM, Azorsa D, Jhun BH, Cheong JH, Lee YC, Meltzer PS, Lee JW (1999). "A nuclear factor, ASC-2, as a cancer-amplified transcriptional coactivator essential for ligand-dependent transactivation by nuclear receptors in vivo". The Journal of Biological Chemistry. 274 (48): 34283–93. doi:10.1074/jbc.274.48.34283. PMID 10567404.
^ Lee SK, Na SY, Jung SY, Choi JE, Jhun BH, Cheong J, Meltzer PS, Lee YC, Lee JW (2000). "Activating protein-1, nuclear factor-kappaB, and serum response factor as novel target molecules of the cancer-amplified transcription coactivator ASC-2". Molecular endocrinology (Baltimore, Md.). 14 (6): 915–25. doi:10.1210/mend.14.6.0471. PMID 10847592.
^ Lee SK, Kim HJ, Na SY, Kim TS, Choi HS, Im SY, Lee JW (1998). "Steroid receptor coactivator-1 coactivates activating protein-1-mediated transactivations through interaction with the c-Jun and c-Fos subunits". The Journal of Biological Chemistry. 273 (27): 16651–4. doi:10.1074/jbc.273.27.16651. PMID 9642216.
^ Wulf GM, Ryo A, Wulf GG, Lee SW, Niu T, Petkova V, Lu KP (2001). "Pin1 is overexpressed in breast cancer and cooperates with Ras signaling in increasing the transcriptional activity of c-Jun towards cyclin D1". The EMBO Journal. 20 (13): 3459–72. doi:10.1093/emboj/20.13.3459. PMC 125530. PMID 11432833.
^ Jung DJ, Na SY, Na DS, Lee JW (2002). "Molecular cloning and characterization of CAPER, a novel coactivator of activating protein-1 and estrogen receptors". Journal of Biological Chemistry. 277 (2): 1229–34. doi:10.1074/jbc.M110417200. PMID 11704680.
^ Nishitani J, Nishinaka T, Cheng CH, Rong W, Yokoyama KK, Chiu R (1999). "Recruitment of the retinoblastoma protein to c-Jun enhances transcription activity mediated through the AP-1 binding site". The Journal of Biological Chemistry. 274 (9): 5454–61. doi:10.1074/jbc.274.9.5454. PMID 10026157.
^ Wertz IE, O'Rourke KM, Zhang Z, Dornan D, Arnott D, Deshaies RJ, Dixit VM (2004). "Human De-etiolated-1 regulates c-Jun by assembling a CUL4A ubiquitin ligase". Science. 303 (5662): 1371–4. Bibcode:2004Sci...303.1371W. doi:10.1126/science.1093549. PMID 14739464.
^ Bianchi E, Denti S, Catena R, Rossetti G, Polo S, Gasparian S, Putignano S, Rogge L, Pardi R (2003). "Characterization of human constitutive photomorphogenesis protein 1, a RING finger ubiquitin ligase that interacts with Jun transcription factors and modulates their transcriptional activity". Journal of Biological Chemistry. 278 (22): 19682–90. doi:10.1074/jbc.M212681200. PMID 12615916.
^ ^a ^b Hess J, Porte D, Munz C, Angel P (2001). "AP-1 and Cbfa/runt physically interact and regulate parathyroid hormone-dependent MMP13 expression in osteoblasts through a new osteoblast-specific element 2/AP-1 composite element". Journal of Biological Chemistry. 276 (23): 20029–38. doi:10.1074/jbc.M010601200. PMID 11274169.
^ ^a ^b D'Alonzo RC, Selvamurugan N, Karsenty G, Partridge NC (2002). "Physical interaction of the activator protein-1 factors c-Fos and c-Jun with Cbfa1 for collagenase-3 promoter activation". Journal of Biological Chemistry. 277 (1): 816–22. doi:10.1074/jbc.M107082200. PMID 11641401.
^ ^a ^b Zhang X, Wrzeszczynska MH, Horvath CM, Darnell JE (1999). "Interacting regions in Stat3 and c-Jun that participate in cooperative transcriptional activation". Molecular and Cellular Biology. 19 (10): 7138–46. PMC 84707. PMID 10490649.
^ ^a ^b Franklin CC, McCulloch AV, Kraft AS (1995). "In vitro association between the Jun protein family and the general transcription factors, TBP and TFIIB". The Biochemical Journal. 305 (Pt 3): 967–74. doi:10.1042/bj3050967. PMC 1136352. PMID 7848298.

External links

c-jun Proteins at the US National Library of Medicine Medical Subject Headings (MeSH)
c-jun Genes at the US National Library of Medicine Medical Subject Headings (MeSH)
Drosophila Jun-related antigen - The Interactive Fly
FactorBook C-Jun

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★リンクテーブル★

拡張検索	「c-jun癌原遺伝子」「c-jun遺伝子」「c-jun gene」
関連記事	「C」「c」

「c-jun癌原遺伝子」

JUN
Available structures
PDB	Ortholog search: PDBe RCSB
List of PDB id codes
	1A02, 1JNM, 1JUN, 1S9K, 1T2K, 1FOS
Identifiers
Aliases	JUN, AP-1, AP1, c-Jun, Jun proto-oncogene, AP-1 transcription factor subunit
External IDs	OMIM: 165160 MGI: 96646 HomoloGene: 1679 GeneCards: JUN
Gene ontology
Molecular function	• GTPase activator activity; • transcription factor activity, sequence-specific DNA binding; • transcriptional activator activity, RNA polymerase II core promoter proximal region sequence-specific binding; • RNA polymerase II activating transcription factor binding; • transcription regulatory region DNA binding; • RNA polymerase II transcription factor activity, sequence-specific DNA binding; • cAMP response element binding; • R-SMAD binding; • HMG box domain binding; • transcription factor binding; • activating transcription factor binding; • RNA polymerase II core promoter proximal region sequence-specific DNA binding; • transcription factor activity, RNA polymerase II core promoter proximal region sequence-specific binding; • enzyme binding; • RNA polymerase II distal enhancer sequence-specific DNA binding; • protein homodimerization activity; • chromatin binding; • transcriptional activator activity, RNA polymerase II transcription factor binding; • protein binding; • double-stranded DNA binding; • DNA binding; • sequence-specific DNA binding; • transcription coactivator activity; • identical protein binding; • protein heterodimerization activity; • transcription factor activity, RNA polymerase II distal enhancer sequence-specific binding; • poly(A) RNA binding;
Cellular component	• cytosol; • transcriptional repressor complex; • nucleus; • nuclear chromosome; • nuclear chromatin; • transcription factor complex; • nucleoplasm; • nuclear euchromatin;
Biological process	• negative regulation of neuron apoptotic process; • negative regulation of DNA binding; • outflow tract morphogenesis; • transcription from RNA polymerase II promoter; • learning; • monocyte differentiation; • response to organic substance; • leading edge cell differentiation; • Fc-epsilon receptor signaling pathway; • positive regulation of neuron apoptotic process; • cellular response to hormone stimulus; • regulation of sequence-specific DNA binding transcription factor activity; • circadian rhythm; • angiogenesis; • positive regulation of ERK1 and ERK2 cascade; • Ras protein signal transduction; • transforming growth factor beta receptor signaling pathway; • negative regulation of cell proliferation; • response to muscle stretch; • cellular response to calcium ion; • response to cytokine; • regulation of transcription, DNA-templated; • SMAD protein signal transduction; • axon regeneration; • SMAD protein import into nucleus; • positive regulation of fibroblast proliferation; • response to mechanical stimulus; • positive regulation of epithelial cell migration; • positive regulation of DNA-templated transcription, initiation; • transcription, DNA-templated; • positive regulation of transcription, DNA-templated; • positive regulation of cell differentiation; • positive regulation of monocyte differentiation; • positive regulation of pri-miRNA transcription from RNA polymerase II promoter; • negative regulation of protein autophosphorylation; • regulation of cell death; • membrane depolarization; • negative regulation of apoptotic process; • eyelid development in camera-type eye; • microglial cell activation; • positive regulation of DNA replication; • negative regulation by host of viral transcription; • response to lipopolysaccharide; • response to radiation; • response to cAMP; • negative regulation of transcription, DNA-templated; • response to hydrogen peroxide; • positive regulation by host of viral transcription; • positive regulation of smooth muscle cell proliferation; • positive regulation of endothelial cell proliferation; • response to organic cyclic compound; • aging; • regulation of cell cycle; • regulation of cell proliferation; • positive regulation of cell proliferation; • positive regulation of apoptotic process; • liver development; • negative regulation of transcription from RNA polymerase II promoter in response to endoplasmic reticulum stress; • cellular response to potassium ion starvation; • response to drug; • cellular process; • release of cytochrome c from mitochondria; • positive regulation of transcription from RNA polymerase II promoter; • positive regulation of GTPase activity;
	Sources:Amigo / QuickGO
RNA expression pattern
	; ; ; ;
	More reference expression data
Orthologs
	3725
	16476
	ENSG00000177606
	ENSMUSG00000052684
	P05412
	P05627
	NM_002228
	NM_010591
	NP_002219.1
	NP_034721.1
	Wikidata
View/Edit Human	View/Edit Mouse

　　[★]

英: c-jun proto-oncogene
関: c-jun遺伝子、jun遺伝子、jun癌原遺伝子

「c-jun遺伝子」

　　[★]

英: c-jun gene
関: jun遺伝子、c-jun癌原遺伝子、jun癌原遺伝子

「c-jun gene」

　　[★]

c-jun遺伝子

関: c-jun proto-oncogene、jun gene、jun proto-oncogene

「C」

　　[★]

炭素 carbon
シトシン cytosine
システイン cysteine
シチジン
セルシウス度摂氏 degrees Celsius degree C
産婦人科領域で「子宮外頚子宮外頚部 exocervix」を表現するための略語

「c」

　　[★]

光速, speed of light

[1] "Human PubMed Reference:".

[2] "Mouse PubMed Reference:".

[3] "Entrez Gene: JUN jun oncogene".

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[pmid17418412-19] Mariani O, Brennetot C, Coindre JM, Gruel N, Ganem C, Delattre O, Stern MH, Aurias A (April 2007). "JUN oncogene amplification and overexpression block adipocytic differentiation in highly aggressive sarcomas". Cancer Cell. 11 (4): 361–74. doi:10.1016/j.ccr.2007.02.007. PMID 17418412.

[pmid17667939-20] Gurzov EN, Bakiri L, Alfaro JM, Wagner EF, Izquierdo M (January 2008). "Targeting Jun and JunB proteins as potential anticancer cell therapy". Oncogene. 27 (5): 641–52. doi:10.1038/sj.onc.1210690. PMID 17667939.

[pmid21789792-21] Kollmann K, Heller G, Sexl V (May 2011). "c-JUN prevents methylation of p16(INK4a) (and Cdk6): the villain turned bodyguard". Oncotarget. 2 (5): 422–7. doi:10.18632/oncotarget.279. PMC 3248190. PMID 21789792.

[pmid23385061-22] Yang CW, Lee YZ, Hsu HY, Wu CM, Chang HY, Chao YS, Lee SJ (March 2013). "c-Jun-mediated anticancer mechanisms of tylophorine". Carcinogenesis. 34 (6): 1304–14. doi:10.1093/carcin/bgt039. PMID 23385061.

[pmid8027667-23] Newell CL, Deisseroth AB, Lopez-Berestein G (1994). "Interaction of nuclear proteins with an AP-1/CRE-like promoter sequence in the human TNF-alpha gene". Journal of leukocyte biology. 56 (1): 27–35. PMID 8027667.

[pmid2320002-24] Kara CJ, Liou HC, Ivashkiv LB, Glimcher LH (1990). "A cDNA for a human cyclic AMP response element-binding protein which is distinct from CREB and expressed preferentially in brain". Molecular and Cellular Biology. 10 (4): 1347–57. PMC 362236. PMID 2320002.

[pmid1827203-25] Hai T, Curran T (1991). "Cross-family dimerization of transcription factors Fos/Jun and ATF/CREB alters DNA binding specificity". Proceedings of the National Academy of Sciences of the United States of America. 88 (9): 3720–4. Bibcode:1991PNAS...88.3720H. doi:10.1073/pnas.88.9.3720. PMC 51524. PMID 1827203.

[pmid9211894-26] Sato N, Sadar MD, Bruchovsky N, Saatcioglu F, Rennie PS, Sato S, Lange PH, Gleave ME (1997). "Androgenic induction of prostate-specific antigen gene is repressed by protein-protein interaction between the androgen receptor and AP-1/c-Jun in the human prostate cancer cell line LNCaP". The Journal of Biological Chemistry. 272 (28): 17485–94. doi:10.1074/jbc.272.28.17485. PMID 9211894.

[pmid12077347-27] Jung DJ, Sung HS, Goo YW, Lee HM, Park OK, Jung SY, Lim J, Kim HJ, Lee SK, Kim TS, Lee JW, Lee YC (2002). "Novel transcription coactivator complex containing activating signal cointegrator 1". Molecular and Cellular Biology. 22 (14): 5203–11. doi:10.1128/MCB.22.14.5203-5211.2002. PMC 139772. PMID 12077347.

[pmid14667575-28] Pearson AG, Gray CW, Pearson JF, Greenwood JM, During MJ, Dragunow M (2003). "ATF3 enhances c-Jun-mediated neurite sprouting". Brain research. Molecular brain research. 120 (1): 38–45. doi:10.1016/j.molbrainres.2003.09.014. PMID 14667575.

[pmid8622660-29] Chen BP, Wolfgang CD, Hai T (1996). "Analysis of ATF3, a transcription factor induced by physiological stresses and modulated by gadd153/Chop10". Molecular and Cellular Biology. 16 (3): 1157–68. doi:10.1128/MCB.16.3.1157. PMC 231098. PMID 8622660.

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[pmid12080089-32] Hu YF, Li R (2002). "JunB potentiates function of BRCA1 activation domain 1 (AD1) through a coiled-coil-mediated interaction". Genes & Development. 16 (12): 1509–17. doi:10.1101/gad.995502. PMC 186344. PMID 12080089.

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