# GADD45G

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{{Short description|Protein-coding gene in the species Homo sapiens}}
{{Infobox_gene}}
'''Growth arrest and DNA-damage-inducible protein GADD45 gamma''' is a [protein](/source/protein) that in humans is encoded by the ''GADD45G'' [gene](/source/gene) on [chromosome 9](/source/chromosome_9). GADD45G is also known as CR6, DDIT2, GRP17, OIG37, and GADD45gamma.<ref name="pmid10496071">{{cite journal | vauthors = Suzuki M, Watanabe TK, Fujiwara T, Takahashi E, Tanigami A | title = Molecular cloning, expression, and mapping of a novel human cDNA, GRP17, highly homologous to human gadd45 and murine MyD118 | journal = J Hum Genet | volume = 44 | issue = 5 | pages = 300–3 | date = Oct 1999 | pmid = 10496071 | doi = 10.1007/s100380050164 | doi-access = free }}</ref> GADD45G is involved in several different processes, including sexual development,<ref name="Johnen_2013">{{cite journal | vauthors = Johnen H, González-Silva L, Carramolino L, Flores JM, Torres M, Salvador JM | title = Gadd45g is essential for primary sex determination, male fertility and testis development | journal = PLOS ONE | volume = 8 | issue = 3 | article-number = e58751 | year = 2013 | pmid = 23516551 | pmc = 3596291 | doi = 10.1371/journal.pone.0058751 | bibcode = 2013PLoSO...858751J | doi-access = free }}</ref> human-specific brain development,<ref name="McLean CY, Reno PL, Pollen AA, et al. 2011 216–9">{{cite journal | vauthors = McLean CY, Reno PL, Pollen AA, Bassan AI, Capellini TD, Guenther C, Indjeian VB, Lim X, Menke DB, Schaar BT, Wenger AM, Bejerano G, Kingsley DM | title = Human-specific loss of regulatory DNA and the evolution of human-specific traits | journal = Nature | volume = 471 | issue = 7337 | pages = 216–9 | date = March 2011 | pmid = 21390129 | pmc = 3071156 | doi = 10.1038/nature09774 | bibcode = 2011Natur.471..216M }}</ref> tumor suppression,<ref name="Tamura">{{cite journal | vauthors = Tamura RE, de Vasconcellos JF, Sarkar D, Libermann TA, Fisher PB, Zerbini LF | title = GADD45 proteins: central players in tumorigenesis | journal = Curr. Mol. Med. | volume = 12 | issue = 5 | pages = 634–51 | date = June 2012 | pmid = 22515981 | pmc = 3797964 | doi =  10.2174/156652412800619978}}</ref> and the [cellular stress response](/source/cellular_stress_response).<ref>{{cite journal | vauthors = Liebermann DA, Hoffman B | title = Gadd45 in the response of hematopoietic cells to genotoxic stress | journal = Blood Cells Mol. Dis. | volume = 39 | issue = 3 | pages = 329–35 | year = 2007 | pmid = 17659913 | pmc = 3268059 | doi = 10.1016/j.bcmd.2007.06.006 }}</ref>  GADD45G interacts with several other proteins that are involved in DNA repair, [cell cycle](/source/cell_cycle) control, [apoptosis](/source/apoptosis), and [senescence](/source/senescence).<ref name="Johnen_2013"/>  Low expression of GADD45G has been associated with many types of [cancer](/source/cancer).<ref name="Zhang_2014">{{cite journal | vauthors = Zhang L, Yang Z, Ma A, Qu Y, Xia S, Xu D, Ge C, Qiu B, Xia Q, Li J, Liu Y | title = Growth arrest and DNA damage 45G down-regulation contributes to Janus kinase/signal transducer and activator of transcription 3 activation and cellular senescence evasion in hepatocellular carcinoma | journal = Hepatology | volume = 59 | issue = 1 | pages = 178–89 | date = January 2014 | pmid = 23897841 | doi = 10.1002/hep.26628 | s2cid = 39582166 | doi-access =  }}</ref>

== History ==

GADD45G was originally cloned by Beadling under the name CR6 in 1993. In this experiment, several genes including GADD45G were noted for being induced by [IL-2](/source/IL-2_receptor), and they were identified as [immediate early response genes](/source/immediate_early_genes) in [T lymphocytes](/source/T_lymphocytes).<ref name="pmid7681987">{{cite journal | vauthors = Beadling C, Johnson KW, Smith KA | title = Isolation of interleukin 2-induced immediate-early genes | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 90 | issue = 7 | pages = 2719–23 | date = April 1993 | pmid = 7681987 | pmc = 46167 | doi = 10.1073/pnas.90.7.2719 | bibcode = 1993PNAS...90.2719B | doi-access = free }}</ref>  Its role as a [tumor suppressor](/source/tumor_suppressor) was discovered in 1999 by Zhang.<ref name="pmid10490824">{{cite journal | vauthors = Zhang W, Bae I, Krishnaraju K, Azam N, Fan W, Smith K, Hoffman B, Liebermann DA | title = CR6: A third member in the MyD118 and Gadd45 gene family which functions in negative growth control | journal = Oncogene | volume = 18 | issue = 35 | pages = 4899–907 | date = September 1999 | pmid = 10490824 | doi = 10.1038/sj.onc.1202885 | s2cid = 24659282 | doi-access =  }}</ref>  It received the name OIG37 from Nakayama due to its regulation by [Oncostatin M](/source/Oncostatin_M), which was found to be able to inhibit growth.<ref name = pmid10455148>{{cite journal | vauthors = Nakayama K, Hara T, Hibi M, Hirano T, Miyajima A | title = A novel oncostatin M-inducible gene OIG37 forms a gene family with MyD118 and GADD45 and negatively regulates cell growth | journal = J. Biol. Chem. | volume = 274 | issue = 35 | pages = 24766–72 | date = August 1999 | pmid = 10455148 | doi = 10.1074/jbc.274.35.24766 | doi-access = free }}</ref>  Finally, it also became known as Gadd-related protein 17 during its isolation from a [cDNA library](/source/cDNA_library) by Suzuki due to its [homology](/source/Homologous_series) with Gadd45.<ref name="pmid10496071"/>

== Structure and function ==

GADD45G is a member of a group of genes whose transcript levels are increased following stressful growth arrest conditions and treatment with DNA-damaging agents. The protein encoded by this gene responds to environmental stresses by mediating activation of the [p38](/source/P38_mitogen-activated_protein_kinases)/[JNK](/source/JNK) pathway via MTK1/[MEKK4](/source/MEKK4) [kinase](/source/kinase).<ref name="pmid9827804">{{cite journal | vauthors = Takekawa M, Saito H | title = A family of stress-inducible GADD45-like proteins mediate activation of the stress-responsive MTK1/MEKK4 MAPKKK | journal = Cell | volume = 95 | issue = 4 | pages = 521–30 | date = Dec 1998 | pmid = 9827804 | doi = 10.1016/S0092-8674(00)81619-0 | s2cid = 18980341 | doi-access = free }}</ref>  GADD45G is in turn regulated upstream by [NF-κB](/source/NF-%CE%BAB).<ref name="Tamura" />

The crystal structure of GADD45G reveals a [dimer](/source/dimer_(chemistry)) made of four parallel helices. The central region contains a highly acidic patch where it allows for interaction with [cdc2](/source/cdc2), [PCNA](/source/PCNA), and [p21](/source/p21). The parallel [isoform](/source/isoform) of GADD45G is the active form.<ref name="pmid22058036">{{cite journal | vauthors = Zhang W, Fu S, Liu X, Zhao X, Zhang W, Peng W, Wu C, Li Y, Li X, Bartlam M, Zeng ZH, Zhan Q, Rao Z | title = Crystal structure of human Gadd45γ [corrected] reveals an active dimer | journal = Protein Cell | volume = 2 | issue = 10 | pages = 814–26 | year = 2011 | pmid = 22058036 | doi = 10.1007/s13238-011-1090-6 | pmc = 4875293 }}</ref>

This gene plays a role in cell cycle regulation. GADD45G prevents the kinase ability of the cyclin b1/[Cdk1](/source/Cdk1) complex in a fashion that does not break apart the complex. It plays a role in the activation of the [S](/source/S_phase) and [G2/M checkpoints](/source/G2_phase).<ref name="Vairapandi_2002">{{cite journal | vauthors = Vairapandi M, Balliet AG, Hoffman B, Liebermann DA | title = GADD45b and GADD45g are cdc2/cyclinB1 kinase inhibitors with a role in S and G2/M cell cycle checkpoints induced by genotoxic stress | journal = J. Cell. Physiol. | volume = 192 | issue = 3 | pages = 327–38 | year = 2002 | pmid = 12124778 | doi = 10.1002/jcp.10140 | s2cid = 19138273 }}</ref>

In the male sexual development pathway, GADD45G is essential for activating [SRY](/source/Testis_determining_factor), leading to proper formation of the [gonads](/source/gonads) and [sex-determination](/source/Sexual_differentiation_in_humans).  This could occur through GADD45G interaction with the [p38](/source/P38_mitogen-activated_protein_kinases) [MAPK signaling pathway](/source/MAPK_signaling_pathway).<ref name="Johnen_2013"/>

Deletion of an [enhancer](/source/Enhancer_(genetics)) close to the GADD45G gene is correlated to increased proliferation of [neuronal](/source/neuronal) cells, which could account for part of the difference in neural development between humans and other species.<ref name="McLean CY, Reno PL, Pollen AA, et al. 2011 216–9"/> The deletion of the enhancer reduces the expression of the gene in the [forebrain](/source/forebrain) allowing for more brain growth in humans.<ref name="IskowGokcumen2012">{{cite journal | vauthors = Iskow RC, Gokcumen O, Lee C | title = Exploring the role of copy number variants in human adaptation | journal = Trends in Genetics | volume = 28 | issue = 6 | pages = 245–257 | year = 2012 | pmid = 22483647 | doi = 10.1016/j.tig.2012.03.002 | issn = 0168-9525 | pmc=3533238}}</ref>

GADD45G is involved with dental [epithelial](/source/epithelial) cell proliferation. GADD45G is expressed in [enamel knots](/source/Enamel_organ), where it regulates gene expression and cell growth. The gene modulates p21-mediated epithelial cell proliferation by activating the p38 MAPK pathway during the development of teeth.<ref name="Ishida_2013">{{cite journal | vauthors = Ishida K, Yuge Y, Hanaoka M, Yasukawa M, Minami Y, Ogawa M, Masumoto KH, Shigeyoshi Y, Saito M, Tsuji T | title = Gadd45g regulates dental epithelial cell proliferation through p38 MAPK-mediated p21 expression | journal = Genes Cells | volume = 18 | issue = 8 | pages = 660–71 | date = August 2013 | pmid = 23751077 | doi = 10.1111/gtc.12067 | s2cid = 23664498 | doi-access = free }}</ref>

There is differential expression of the [Xenopus](/source/Xenopus) homolog of GADD45G in embryonic development. It plays a large role in neural and brain development with [GADD45A](/source/GADD45A). GADD45G and GADD45A [knockdowns](/source/Genetic_knockout) are related to improper [gastrulation](/source/gastrulation), defective head growth, and shorter axes. GADD45G and GADD45A act [redundantly](/source/Genetic_redundancy) to control cell growth, allow the cells to move from [pluripotency](/source/pluripotent) helping [cells differentiate](/source/Cell_differentiation).<ref name="KaufmannNiehrs2011">{{cite journal | vauthors = Kaufmann LT, Niehrs C | title = Gadd45a and Gadd45g regulate neural development and exit from pluripotency in Xenopus | journal = Mechanisms of Development | volume = 128 | issue = 7–10 | pages = 401–411 | year = 2011 | pmid = 21854844 | doi = 10.1016/j.mod.2011.08.002 | issn = 0925-4773 | doi-access = free }}</ref>

===Memory===

During a learning experience, a set of genes is rapidly expressed in the [brain](/source/brain).  This induced gene expression is thought to be important for processing the information being learned.  Such genes are known as [immediate early gene](/source/immediate_early_gene)s.  Within the prelimbic [prefrontal cortex](/source/prefrontal_cortex), the ''GADD45G'' gene is immediately expressed and is required for the consolidation of a type of learning in mice termed [associative fear memory](/source/fear_conditioning).<ref name =Li2019>{{cite journal | vauthors = Li X, Marshall PR, Leighton LJ, Zajaczkowski EL, Wang Z, Madugalle SU, Yin J, Bredy TW, Wei W | display-authors = 6 | title = The DNA Repair-Associated Protein Gadd45γ Regulates the Temporal Coding of Immediate Early Gene Expression within the Prelimbic Prefrontal Cortex and Is Required for the Consolidation of Associative Fear Memory | journal = The Journal of Neuroscience | volume = 39 | issue = 6 | pages = 970–983 | date = February 2019 | pmid = 30545945 | pmc = 6363930 | doi = 10.1523/JNEUROSCI.2024-18.2018 }}</ref>  In general, [gene expression](/source/gene_expression) often can be [epigenetic](/source/epigenetic)ally induced by [demethylation](/source/DNA_demethylation) of [5-methylcytosine](/source/5-methylcytosine)(s) in [gene promoter](/source/promoter_(genetics)) regions.  The GADD45G protein functions in [repair of DNA damage](/source/DNA_repair). GADD45G may also be involved in recognition of 5-methylcytosine as an alteration in DNA that needs to be repaired to allow induction of learning-related genes.  Thus GADD45G may guide the rapid demethylation of methylcytosine in the promoter regions of learning-related genes by a [DNA repair](/source/DNA_repair) process<ref name =Li2019/>(see also [Epigenetics in learning and memory](/source/Epigenetics_in_learning_and_memory)).

== Interactions ==

GADD45G carries out its many previously stated functions with many different interactions.  GADD45G was found to inhibit [Cdk1 kinase](/source/Cdk1) activity, which would cause disruption of cell growth.<ref name="Vairapandi_2002"/>  It also interacts with CRIF, which causes the inhibition of Cdc2-cyclin B1 and Cdk-cyclin E.<ref>{{cite journal | vauthors = Chung HK, Yi YW, Jung NC, Kim D, Suh JM, Kim H, Park KC, Song JH, Kim DW, Hwang ES, Yoon SH, Bae YS, Kim JM, Bae I, Shong M | title = CR6-interacting factor 1 interacts with Gadd45 family proteins and modulates the cell cycle | journal = J. Biol. Chem. | volume = 278 | issue = 30 | pages = 28079–88 | date = July 2003 | pmid = 12716909 | doi = 10.1074/jbc.M212835200 | doi-access = free }}</ref>  GADD45 also works with the cyclin-dependent kinase inhibitor [p21](/source/p21), which can cause growth arrest as well.<ref name = pmid11022036/>  GADD45G is found to be involved with the [p38](/source/P38_mitogen-activated_protein_kinases) MAPK pathway through interactions with [MAP3K4](/source/MAP3K4), which can be important in sex-determination.<ref>{{cite journal | vauthors = Warr N, Carre GA, Siggers P, Faleato JV, Brixey R, Pope M, Bogani D, Childers M, Wells S, Scudamore CL, Tedesco M, del Barco Barrantes I, Nebreda AR, Trainor PA, Greenfield A | title = Gadd45γ and Map3k4 interactions regulate mouse testis determination via p38 MAPK-mediated control of Sry expression | journal = Dev. Cell | volume = 23 | issue = 5 | pages = 1020–31 | date = November 2012 | pmid = 23102580 | pmc = 3526779 | doi = 10.1016/j.devcel.2012.09.016 }}</ref>  Additionally, GADD45G regulates DNA replication and repair through its interactions with [PCNA](/source/PCNA).<ref name = pmid10455148 /><ref name = pmid11022036>{{cite journal | vauthors = Azam N, Vairapandi M, Zhang W, Hoffman B, Liebermann DA | title = Interaction of CR6 (GADD45gamma ) with proliferating cell nuclear antigen impedes negative growth control | journal = J. Biol. Chem. | volume = 276 | issue = 4 | pages = 2766–74 | date = Jan 2001 | pmid = 11022036 | doi = 10.1074/jbc.M005626200 | doi-access = free }}</ref>

== Tissue distribution ==
In humans, GADD45G is expressed most in the [skeletal muscle](/source/skeletal_muscle), [kidney](/source/kidney) and [liver](/source/liver). This gene has a low expression in the [heart](/source/heart), [brain](/source/brain), [spleen](/source/spleen), [lung](/source/lung) and testis.<ref name="Tamura" />  GADD45G is highly expressed in the placenta.<ref name="entrez">{{cite web | title = Entrez Gene: GADD45G growth arrest and DNA-damage-inducible, gamma| url = https://www.ncbi.nlm.nih.gov/gene?Db=gene&Cmd=ShowDetailView&TermToSearch=10912}}</ref>

In the embryonic mouse, Gadd45g is expressed in the [neural tube](/source/neural_tube), [cranial](/source/Cranial_nerves) and [dorsal root ganglia](/source/Dorsal_root_ganglion) and the [dorsal](/source/Dorsal_(anatomy)) [midbrain](/source/midbrain).<ref name="KaufmannGierl2011">{{cite journal | vauthors = Kaufmann LT, Gierl MS, Niehrs C | title = Gadd45a, Gadd45b and Gadd45g expression during mouse embryonic development | journal = Gene Expression Patterns | volume = 11 | issue = 8 | pages = 465–470 | year = 2011 | pmid = 21843656 | doi = 10.1016/j.gep.2011.07.005 | issn = 1567-133X }}</ref>

Mammalian renal inner medullary (IM) cells routinely face and resist hypertonic stress. Such stress causes DNA damage to which IM cells respond with cell cycle arrest. All three [GADD45](/source/GADD45) isoforms [GADD45A](/source/GADD45A), [GADD45B](/source/GADD45B), and GADD45G are induced by acute hypertonicity in murine IM cells. Maximum induction occurs 16-18 h after the onset of hypertonicity. GADD45G is induced more strongly (7-fold) than [GADD45B](/source/GADD45B) (3-fold) and [GADD45A](/source/GADD45A) (2-fold).  Hypertonicity of various forms (NaCl, KCl, sorbitol, or mannitol) always induces [GADD45](/source/GADD45) transcripts, whereas non-hypertonic hyperosmolality (urea) has no effect. Actinomycin D does not prevent hypertonic GADD45 induction, indicating that mRNA stabilization is the mechanism that mediates this induction.<ref name="Chakravarty_2002">{{cite journal | vauthors = Chakravarty D, Cai Q, Ferraris JD, Michea L, Burg MB, Kültz D | title = Three GADD45 isoforms contribute to hypertonic stress phenotype of murine renal inner medullary cells | journal = American Journal of Physiology. Renal Physiology | volume = 283 | issue = 5 | pages = F1020–9 | date = November 2002 | pmid = 12372778 | doi = 10.1152/ajprenal.00118.2002 }}</ref>

== Clinical significance ==

In numerous kinds of cancerous cells, GADD45G is [down regulated](/source/Down-regulation).<ref name="Zhang_2014"/> There is a low expression due to [methylation](/source/methylation) of the GADD45G promoter.<ref name="Ishida_2013"/>  This low expression can also be explained by increased NF-κB activation.<ref name="pmid22150313">{{cite journal | vauthors = Liebermann DA, Tront JS, Sha X, Mukherjee K, Mohamed-Hadley A, Hoffman B | title = Gadd45 stress sensors in malignancy and leukemia | journal = Crit Rev Oncog | volume = 16 | issue = 1–2 | pages = 129–40 | year = 2011 | pmid = 22150313 | pmc = 3268054 | doi = 10.1615/critrevoncog.v16.i1-2.120 }}</ref>

GADD45G methylation is seen in many cancers. In [esophageal cancer](/source/esophageal_cancer) the expression level and methylation status of the gene are involved in the prognosis of esophageal [squamous cell carcinoma](/source/squamous_cell_carcinoma). Demethylation of the gene can have some beneficial effects.<ref name="Ishida_2013"/> Similar circumstances are seen in [gastric cardio adenocarcinomas](/source/Gastric_cancer) where GADD45G is silenced.<ref name="GuoDong2013">{{cite journal | vauthors = Guo W, Dong Z, Guo Y, Chen Z, Kuang G, Yang Z | title = Methylation-mediated repression of GADD45A and GADD45G expression in gastric cardia adenocarcinoma | journal = International Journal of Cancer | volume = 133 | issue = 9 | pages = 2043–2053 | year = 2013 | pmid = 23616123 | doi = 10.1002/ijc.28223 | s2cid = 36324243 | issn = 0020-7136 | doi-access = free }}</ref> GADD45G methylation levels are also measured in the diagnosis of pancreatic and colorectal cancers.<ref name="pmid20111973">{{cite journal | vauthors = Zhang W, Li T, Shao Y, Zhang C, Wu Q, Yang H, Zhang J, Guan M, Yu B, Wan J | title = Semi-quantitative detection of GADD45-gamma methylation levels in gastric, colorectal and pancreatic cancers using methylation-sensitive high-resolution melting analysis | journal = J. Cancer Res. Clin. Oncol. | volume = 136 | issue = 8 | pages = 1267–73 | date = August 2010 | pmid = 20111973 | doi = 10.1007/s00432-010-0777-z | s2cid = 37780631 | pmc = 11828201 }}</ref>

In the [pituitary gland](/source/pituitary_gland), GADD45G is a growth suppressor. There is a loss of expression of the gene in many pituitary cancerous masses.<ref name="pmid11889197">{{cite journal | vauthors = Zhang X, Sun H, Danila DC, Johnson SR, Zhou Y, Swearingen B, Klibanski A | title = Loss of expression of GADD45 gamma, a growth inhibitory gene, in human pituitary adenomas: implications for tumorigenesis | journal = J Clin Endocrinol Metab | volume = 87 | issue = 3 | pages = 1262–7 | year = 2002 | doi = 10.1210/jcem.87.3.8315 | pmid = 11889197 | doi-access = free }}</ref> The gene plays a role in [prostate cancer](/source/prostate_cancer) as a tumor suppressor as well. In these cancerous cells, [Vitamin D](/source/Vitamin_D) can induce the expression of GADD45G.<ref name="pmid20739400">{{cite journal | vauthors = Flores O, Burnstein KL | title = GADD45gamma: a new vitamin D-regulated gene that is antiproliferative in prostate cancer cells | journal = Endocrinology | volume = 151 | issue = 10 | pages = 4654–64 | year = 2010 | pmid = 20739400 | pmc = 2946153 | doi = 10.1210/en.2010-0434 }}</ref> GADD45G could possibly be a target of therapeutic benefit for prostate cancer.<ref>{{cite journal | vauthors = Liebermann DA, Hoffman B | title = Prostate cancer: JunD, Gadd45a and Gadd45g as therapeutic targets | journal = Cell Cycle | volume = 10 | issue = 20 | page = 3428 | date = October 2011 | pmid = 22030693 | doi = 10.4161/cc.10.20.17528 | doi-access = free }}</ref>

In [cancerous liver cells](/source/Liver_cancer), GADD45G is down regulated. It participates in negatively regulating the JAK-STAT3 signaling pathway. It acts as a tumor suppressor in [HCC](/source/Hepatic_carcinoma) cells by promoting cell death or growth arrest. When GADD45G expression is low, liver cells may be able to bypass the growth arrest stage, leading to cancerous cells.<ref name="Zhang_2014"/>

The presence of GADD45G in the [urinary system](/source/urinary_system) is also related to [renal disease](/source/renal_disease). The renal cells expressing the gene were damaged.<ref name="pmid19293565">{{cite journal | vauthors = Yu S, Cho J, Park I, Kim SJ, Kim H, Shin GT | title = Urinary GADD45gamma expression is associated with progression of lgA nephropathy | journal = Am J Nephrol | volume = 30 | issue = 2 | pages = 135–9 | year = 2009 | doi = 10.1159/000209317 | pmid = 19293565 | s2cid = 46326535 }}</ref>

The upregulation of Gadd45g due to hormones may account for the changes in the mouse uterus.<ref name="IvangaLabrie2009">{{cite journal | vauthors = Ivanga M, Labrie Y, Calvo E, Belleau P, Martel C, Pelletier G, Morissette J, Labrie F, Durocher F | title = Fine temporal analysis of DHT transcriptional modulation of the ATM/Gadd45g signaling pathways in the mouse uterus | journal = Molecular Reproduction and Development | volume = 76 | issue = 3 | pages = 278–288 | year = 2009 | pmid = 18671277 | doi = 10.1002/mrd.20949 | s2cid = 9149501 | issn = 1040-452X }}</ref>

== See also==
*[Gadd45](/source/Gadd45)  
*[GADD45A](/source/GADD45A)
*[GADD45B](/source/GADD45B)

== References ==
{{reflist|35em}}

==Further reading==
{{refbegin|35em}}
* {{cite journal | vauthors = Fan W, Richter G, Cereseto A, Beadling C, Smith KA | title = Cytokine response gene 6 induces p21 and regulates both cell growth and arrest | journal = Oncogene | volume = 18 | issue = 47 | pages = 6573–82 | year = 2000 | pmid = 10597261 | doi = 10.1038/sj.onc.1203054 | doi-access = free }}
* {{cite journal | vauthors = Gong R, Yu L, Zhang H, Tu Q, Zhao Y, Yang J, Xu Y, Zhao S | title = Assignment of human GADD45G to chromosome 9q22.1→q22.3 by radiation hybrid mapping | journal = Cytogenet. Cell Genet. | volume = 88 | issue = 1–2 | pages = 95–6 | year = 2000 | pmid = 10773677 | doi = 10.1159/000015496 | s2cid = 45495955 }}
* {{cite journal | vauthors = Yi YW, Kim D, Jung N, Hong SS, Lee HS, Bae I | title = Gadd45 family proteins are coactivators of nuclear hormone receptors | journal = Biochem. Biophys. Res. Commun. | volume = 272 | issue = 1 | pages = 193–8 | year = 2000 | pmid = 10872826 | doi = 10.1006/bbrc.2000.2760 }}
* {{cite journal | vauthors = Yang Q, Manicone A, Coursen JD, Linke SP, Nagashima M, Forgues M, Wang XW | title = Identification of a functional domain in a GADD45-mediated G2/M checkpoint | journal = J. Biol. Chem. | volume = 275 | issue = 47 | pages = 36892–8 | year = 2001 | pmid = 10973963 | doi = 10.1074/jbc.M005319200 | doi-access = free }}
* {{cite journal | vauthors = Wan Y, Wang Z, Shao Y, Xu Y, Voorhees J, Fisher G | title = UV-induced expression of GADD45 is mediated by an oxidant sensitive pathway in cultured human keratinocytes and in human skin in vivo | journal = Int. J. Mol. Med. | volume = 6 | issue = 6 | pages = 683–8 | year = 2001 | pmid = 11078829 | doi = 10.3892/ijmm.6.6.683 }}
* {{cite journal | vauthors = Kovalsky O, Lung FD, Roller PP, Fornace AJ | title = Oligomerization of human Gadd45a protein | journal = J. Biol. Chem. | volume = 276 | issue = 42 | pages = 39330–9 | year = 2001 | pmid = 11498536 | doi = 10.1074/jbc.M105115200 | doi-access = free }}
* {{cite journal | vauthors = Sun L, Gong R, Wan B, Huang X, Wu C, Zhang X, Zhao S, Yu L | title = GADD45gamma, down-regulated in 65% hepatocellular carcinoma (HCC) from 23 Chinese patients, inhibits cell growth and induces cell cycle G2/M arrest for hepatoma Hep-G2 cell lines | journal = Mol. Biol. Rep. | volume = 30 | issue = 4 | pages = 249–53 | year = 2004 | pmid = 14672412 | doi = 10.1023/A:1026370726763 | s2cid = 33065335 }}
* {{cite journal | vauthors = Jiang F, Wang Z | title = Gadd45gamma is androgen-responsive and growth-inhibitory in prostate cancer cells | journal = Mol. Cell. Endocrinol. | volume = 213 | issue = 2 | pages = 121–9 | year = 2004 | pmid = 15062559 | doi = 10.1016/j.mce.2003.10.050 | s2cid = 54408868 }}
* {{cite journal | vauthors = Zerbini LF, Wang Y, Czibere A, Correa RG, Cho JY, Ijiri K, Wei W, Joseph M, Gu X, Grall F, Goldring MB, Zhou JR, Libermann TA, Zhou JR | title = NF-kappa B-mediated repression of growth arrest- and DNA-damage-inducible proteins 45alpha and gamma is essential for cancer cell survival | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 101 | issue = 37 | pages = 13618–23 | year = 2004 | pmid = 15353598 | pmc = 518803 | doi = 10.1073/pnas.0402069101 | bibcode = 2004PNAS..10113618Z | doi-access = free }}
* {{cite journal|author23-link=Bernhard Landwehrmeyer | vauthors = Goehler H, Lalowski M, Stelzl U, Waelter S, Stroedicke M, Worm U, Droege A, Lindenberg KS, Knoblich M, Haenig C, Herbst M, Suopanki J, Scherzinger E, Abraham C, Bauer B, Hasenbank R, Fritzsche A, Ludewig AH, Büssow K, Buessow K, Coleman SH, Gutekunst CA, Landwehrmeyer BG, Lehrach H, Wanker EE | title = A protein interaction network links GIT1, an enhancer of huntingtin aggregation, to Huntington's disease | journal = Mol. Cell | volume = 15 | issue = 6 | pages = 853–65 | year = 2004 | pmid = 15383276 | doi = 10.1016/j.molcel.2004.09.016 | doi-access = free }}
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Adapted from the Wikipedia article [GADD45G](https://en.wikipedia.org/wiki/GADD45G) by Wikipedia contributors ([contributor history](https://en.wikipedia.org/wiki/GADD45G?action=history)). Available under [Creative Commons Attribution-ShareAlike 4.0 International](https://creativecommons.org/licenses/by-sa/4.0/). Changes may have been made.
