BTG2

Last updated
BTG2
Protein BTG2 PDB 3DJU.png
Available structures
PDB Ortholog search: PDBe RCSB
Identifiers
Aliases BTG2 , PC3, TIS21, BTG family member 2, BTG anti-proliferation factor 2, APRO1
External IDs OMIM: 601597 MGI: 108384 HomoloGene: 31406 GeneCards: BTG2
Orthologs
SpeciesHumanMouse
Entrez

7832

12227

Ensembl

ENSG00000159388

ENSMUSG00000020423

UniProt

P78543

Q04211

RefSeq (mRNA)

NM_006763

NM_007570

RefSeq (protein)

NP_006754

NP_031596

Location (UCSC) Chr 1: 203.31 – 203.31 Mb n/a
PubMed search [2] [3]
Wikidata
View/Edit Human View/Edit Mouse

Protein BTG2 also known as BTG family member 2 or NGF-inducible anti-proliferative protein PC3 or NGF-inducible protein TIS21, is a protein that in humans is encoded by the BTG2 gene (B-cell translocation gene 2) [4] and in other mammals by the homologous Btg2 gene. [5] [6] This protein controls cell cycle progression and proneural genes expression by acting as a transcription coregulator that enhances or inhibits the activity of transcription factors.

Contents

The protein BTG2 is the human homolog of the PC3 (pheochromocytoma cell 3) protein in rat and of the Tis21 (tetradecanoyl phorbol acetate-inducible sequence 21) protein in mouse. [7] [8] Tis21 had been originally isolated as a sequence induced by TPA in mouse fibroblasts, [6] whereas PC3 was originally isolated as sequence induced at the beginning of neuron differentiation; [5] BTG2 was then isolated in human cells as sequence induced by p53 and DNA damage. [4] [9]

The protein encoded by the gene BTG2 (which is the official name assigned to the gene PC3/Tis21/BTG2) is a member of the BTG/Tob family (that comprises six proteins BTG1, BTG2/PC3/Tis21, BTG3/ANA, BTG4/PC3B, Tob1/Tob and Tob2). [7] [8] [10] This family has structurally related proteins that appear to have antiproliferative properties. In particular, the BTG2 protein has been shown to negatively control a cell cycle checkpoint at the G1 to S phase transition in fibroblasts and neuronal cells by direct inhibition of the activity of cyclin D1 promoter. [11] [12] [13]

Regulator of neuron differentiation

A number of studies in vivo have shown that BTG2 expression is associated with the neurogenic asymmetric division in neural progenitor cells. [14] [15] [16] [17] [18] Tis21-GFP has been used as a neurogenic marker because it is not expressed until neurogenesis begins, is present in almost all early-born neurons, and interacts with neuron producing intermediate progenitor cells. [19] Moreover, when directly overexpressed in vivo in neural progenitor cells, BTG2 induces their differentiation. [20] [21] In fact, in the neuronal PC12 cell line BTG2 is not able to trigger differentiation by itself, but only to synergize with NGF, [22] [23] while in vivo BTG2 is fully able to induce differentiation of progenitor cells, i.e., during embryonic development in the neuroblast of the neural tube and in granule precursors of cerebellum, as well in adult progenitor cells of the dentate gyrus and of the subventricular zone. [20] [21] Notably, it has recently been shown that BTG2 is essential for the differentiation of new neurons, using a BTG2 knock out mouse. [24] BTG2 is thus a pan-neural gene required for the development of the new neurons generated during adulthood, in the two neurogenic regions of adult brain, i.e., the hippocampus and the subventricular zone. [24] Such requirement of BTG2 in neuron maturation is consistent with the fact that during brain development BTG2 is expressed in the proliferating neuroblasts of the ventricular zone of the neural tube, and to a lower extent in the differentiating neuroblasts of the mantle zone; postnatally it is expressed in cerebellar precursors mainly in the proliferating regions of the neuropithelium (i.e., in the external granular layer), and in the hippocampus in proliferating and differentiating progenitor cells. [14] [20] [21] The pro-differentiative action of BTG2 appears to be consequent not only to inhibition of cell cycle progression but also to a BTG2-dependent activation of proneural genes in neural progenitor cells. [20] [24] In fact, BTG2 activates proneural genes by associating with the promoter of Id3, a key inhibitor of proneural gene activity, and by negatively regulating its activity. [24]

BTG2 is a transcriptional cofactor, given that it has been shown to associate with, and regulate the promoters not only of Id3 but also of cyclin D1 and RAR-β, being part of transcriptional complexes. [13] [25] [26] It has been shown that when the differentiation of new neurons of the hippocampus - a brain region important for learning and memory - is either accelerated or delayed by means of overexpression or deletion of BTG2, respectively, spatial and contextual memory is heavily altered. [21] [24] This suggests that the time the young neurons spend in different states of neuronal differentiation is critical for their ultimate function in learning and memory, and that BTG2 may play a role in the timing of recruitment of the new neuron into memory circuits. [21] [24]

In conclusion, the main action of Btg2 on neural progenitor cells of the dentate gyrus and subventricular zone during adult neurogenesis is the positive control of their terminal differentiation (see for review: [27] ). During the early postnatal development of the cerebellum, Btg2 is mainly required to control the migration and differentiation of the precursor cells of cerebellar granule neurons. [28] In contrast, BTG1, the closest homolog to Btg2, appears to negatively regulate the proliferation of adult stem cells in the dentate gyrus and subventricular zone, maintaining in quiescence the stem cells pool and preserving it from depletion. [29] [30] BTG1 is also necessary to limit the proliferative expansion of cerebellar precursor cells, as without BTG1 the adult cerebellum is larger and unable to coordinate motor activity. [31]

Medulloblastoma suppressor

BTG2 has been shown to inhibit medulloblastoma, the very aggressive tumor of cerebellum, by inhibiting the proliferation and triggering the differentiation of the precursors of cerebellar granule neurons. This demonstration was obtained by overexpressing BTG2 in a mouse model of medulloblastoma, presenting activation of the sonic hedgehog pathway (heterozygous for the gene Patched1). [13] More recently, it has been shown that the ablation of BTG2 greatly enhances the medulloblastoma frequency by inhibiting the migration of cerebellar granule neuron precursors. This impairment of migration of the precursors of cerebellar granule neurons forces them to remain at the surface of the cerebellum, where they continue to proliferate, becoming target of transforming insults. [32] The impairment of migration of the precursors of cerebellar granule neurons (GCPs) depends on the inhibition of expression of the chemokine CXCL3 consequent to ablation of BTG2. In fact, the transcription of CXCL3 is directly regulated by BTG2, and CXCL3 is able to induce cell-autonomously the migration of cerebellar granule precursors. Treatment with CXCL3 prevents the growth of medulloblastoma lesions in a Shh-type mouse model of medulloblastoma. [33] Thus, CXCL3 is a target for medulloblastoma therapy. [32] [33]

Interactions

BTG2 has been shown to interact with PRMT1, [26] HOXB9, [34] [35] CNOT8 [36] and HDAC1 HDAC4 and HDAC9. [37] [13] It has also been studied with Pax6 and Tbr2 when observing the role of Tis21 in neurogenic divisions. [19]

Related Research Articles

Cellular differentiation Process in which relatively unspecialized cells acquire specialized features

Cellular differentiation is the process in which a cell changes from one cell type to another. Usually, the cell changes to a more specialized type. Differentiation occurs numerous times during the development of a multicellular organism as it changes from a simple zygote to a complex system of tissues and cell types. Differentiation continues in adulthood as adult stem cells divide and create fully differentiated daughter cells during tissue repair and during normal cell turnover. Some differentiation occurs in response to antigen exposure. Differentiation dramatically changes a cell's size, shape, membrane potential, metabolic activity, and responsiveness to signals. These changes are largely due to highly controlled modifications in gene expression and are the study of epigenetics. With a few exceptions, cellular differentiation almost never involves a change in the DNA sequence itself. Although metabolic composition does get altered quite dramatically where stem cells are characterized by abundant metabolites with highly unsaturated structures whose levels decrease upon differentiation. Thus, different cells can have very different physical characteristics despite having the same genome.

MyoD

MyoD, also known as myoblast determination protein 1, is a protein in animals that plays a major role in regulating muscle differentiation. MyoD, which was discovered in the laboratory of Harold M. Weintraub, belongs to a family of proteins known as myogenic regulatory factors (MRFs). These bHLH transcription factors act sequentially in myogenic differentiation. Vertebrate MRF family members include MyoD1, Myf5, myogenin, and MRF4 (Myf6). In non-vertebrate animals, a single MyoD protein is typically found.

Medulloblastoma Most common type of primary brain cancer in children

Medulloblastoma is a common type of primary brain cancer in children. It originates in the part of the brain that is towards the back and the bottom, on the floor of the skull, in the cerebellum, or posterior fossa.

Bone morphogenetic protein 4

Bone morphogenetic protein 4 is a protein that in humans is encoded by BMP4 gene. BMP4 is found on chromosome 14q22-q23

CXCL3

Chemokine ligand 3 (CXCL3) is a small cytokine belonging to the CXC chemokine family that is also known as GRO3 oncogene (GRO3), GRO protein gamma (GROg) and macrophage inflammatory protein-2-beta (MIP2b). CXCL3 controls migration and adhesion of monocytes and mediates its effects on its target cell by interacting with a cell surface chemokine receptor called CXCR2. More recently, it has been shown that Cxcl3 regulates cell autonomously the migration of the precursors of cerebellar granule neurons toward the internal layers of cerebellum, during the morphogenesis of cerebellum. Moreover, if the expression of Cxcl3 is reduced in cerebellar granule neuron precursors, this highly enhances the frequency of the medulloblastoma, the tumor of cerebellum. In fact, the reduced expression of Cxcl3 forces the cerebellar granule neuron precursors to remain at the surface of the cerebellum, where they highly proliferate under the stimulus of Sonic hedgehog, becoming target of transforming insults. Remarkably, the treatment with CXCL3 completely prevents the growth of medulloblastoma lesions in a Shh-type mouse model of medulloblastoma. Thus, CXCL3 is a target for medulloblastoma therapy. Cxcl3 is directly regulated transcriptionally by BTG2

HDAC4

Histone deacetylase 4, also known as HDAC4, is a protein that in humans is encoded by the HDAC4 gene.

ID3 (gene)

DNA-binding protein inhibitor ID-3 is a protein that in humans is encoded by the ID3 gene.

HDAC9

Histone deacetylase 9 is an enzyme that in humans is encoded by the HDAC9 gene.

HOXC8

Homeobox protein Hox-C8 is a protein that in humans is encoded by the HOXC8 gene.

TOB1

Protein Tob1 is a protein that in humans is encoded by the TOB1 gene.

HOXB9

Homeobox protein Hox-B9 is a protein that in humans is encoded by the HOXB9 gene.

IFRD1

Interferon-related developmental regulator 1 is a protein that in humans is encoded by the IFRD1 gene. The gene is expressed mostly in neutrophils, skeletal and cardiac muscle, brain, pancreas. The rat and the mouse homolog genes of interferon-related developmental regulator 1 gene are also known with the name PC4 and Tis21, respectively. IFRD1 is member of a gene family that comprises a second gene, IFRD2, also known as SKmc15.

CNOT7

CCR4-NOT transcription complex subunit 7 is a protein that in humans is encoded by the CNOT7 gene. It is a subunit of the CCR4-Not deadenylase complex.

BTG1

Protein BTG1 is a protein that in humans is encoded by the BTG1 gene.

ATOH1

Protein atonal homolog 1 is a protein that in humans is encoded by the ATOH1 gene.

Neurogenins are a family of bHLH transcription factors involved in specifying neuronal differentiation. It is one of many gene families related to the atonal gene in Drosophila. Other positive regulators of neuronal differentiation also expressed during early neural development include NeuroD and ASCL1.

ZNF238

Zinc finger protein 238 is a zinc finger containing transcription factor that in humans is encoded by the ZNF238 gene.

BTG3

Protein BTG3 is a protein that in humans is encoded by the BTG3 gene.

TBR1 Protein-coding gene in Homo sapiens

T-box, brain, 1 is a transcription factor protein important in vertebrate embryo development. It is encoded by the TBR1 gene. This gene is also known by several other names: T-Brain 1, TBR-1, TES-56, and MGC141978. TBR1 is a member of the TBR1 subfamily of T-box family transcription factors, which share a common DNA-binding domain. Other members of the TBR1 subfamily include EOMES and TBX21. TBR1 is involved in the differentiation and migration of neurons and is required for normal brain development. TBR1 interacts with various genes and proteins in order to regulate cortical development, specifically within layer VI of the developing six-layered human cortex. Studies show that TBR1 may play a role in major neurological diseases such as Alzheimer's disease (AD), Parkinson's disease (PD) and autism spectrum disorder (ASD).

BTG4

Protein BTG4 also known as BTG family member 4 is a protein that in humans is encoded by the BTG4 gene (B-cell translocation gene 4). BTG4 has anti-proliferative properties and can induce G1 cell cycle arrest.

References

  1. 1 2 3 GRCh38: Ensembl release 89: ENSG00000159388 - Ensembl, May 2017
  2. ↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  3. ↑ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. 1 2 Rouault JP, Falette N, Guéhenneux F, Guillot C, Rimokh R, Wang Q, Berthet C, Moyret-Lalle C, Savatier P, Pain B, Shaw P, Berger R, Samarut J, Magaud JP, Ozturk M, Samarut C, Puisieux A (December 1996). "Identification of BTG2, an antiproliferative p53-dependent component of the DNA damage cellular response pathway". Nature Genetics. 14 (4): 482–6. doi:10.1038/ng1296-482. hdl: 11693/49026 . PMID   8944033. S2CID   20119529.
  5. 1 2 Bradbury A, Possenti R, Shooter EM, Tirone F (April 1991). "Molecular cloning of PC3, a putatively secreted protein whose mRNA is induced by nerve growth factor and depolarization". Proceedings of the National Academy of Sciences of the United States of America. 88 (8): 3353–7. Bibcode:1991PNAS...88.3353B. doi: 10.1073/pnas.88.8.3353 . PMC   51445 . PMID   1849653.
  6. 1 2 Fletcher BS, Lim RW, Varnum BC, Kujubu DA, Koski RA, Herschman HR (August 1991). "Structure and expression of TIS21, a primary response gene induced by growth factors and tumor promoters". The Journal of Biological Chemistry. 266 (22): 14511–8. doi: 10.1016/S0021-9258(18)98716-8 . PMID   1713584.
  7. 1 2 Matsuda S, Rouault J, Magaud J, Berthet C (May 2001). "In search of a function for the TIS21/PC3/BTG1/TOB family". FEBS Letters. 497 (2–3): 67–72. doi: 10.1016/S0014-5793(01)02436-X . PMID   11377414.
  8. 1 2 Tirone F (May 2001). "The gene PC3(TIS21/BTG2), prototype member of the PC3/BTG/TOB family: regulator in control of cell growth, differentiation, and DNA repair?". Journal of Cellular Physiology. 187 (2): 155–65. doi: 10.1002/jcp.1062 . PMID   11267995.
  9. ↑ "Entrez Gene: BTG2 BTG family, member 2".
  10. ↑ Winkler GS (January 2010). "The mammalian anti-proliferative BTG/Tob protein family". Journal of Cellular Physiology. 222 (1): 66–72. doi:10.1002/jcp.21919. PMID   19746446. S2CID   3436967.
  11. ↑ Montagnoli A, Guardavaccaro D, Starace G, Tirone F (October 1996). "Overexpression of the nerve growth factor-inducible PC3 immediate early gene is associated with growth inhibition". Cell Growth & Differentiation. 7 (10): 1327–36. PMID   8891336.
  12. ↑ Guardavaccaro D, Corrente G, Covone F, Micheli L, D'Agnano I, Starace G, Caruso M, Tirone F (March 2000). "Arrest of G(1)-S progression by the p53-inducible gene PC3 is Rb dependent and relies on the inhibition of cyclin D1 transcription". Molecular and Cellular Biology. 20 (5): 1797–815. doi:10.1128/MCB.20.5.1797-1815.2000. PMC   85361 . PMID   10669755.
  13. 1 2 3 4 Farioli-Vecchioli S, Tanori M, Micheli L, Mancuso M, Leonardi L, Saran A, Ciotti MT, Ferretti E, Gulino A, Pazzaglia S, Tirone F (July 2007). "Inhibition of medulloblastoma tumorigenesis by the antiproliferative and pro-differentiative gene PC3" (PDF). FASEB Journal. 21 (9): 2215–25. doi:10.1096/fj.06-7548com. PMID   17371797. S2CID   4974360.
  14. 1 2 Iacopetti P, Barsacchi G, Tirone F, Maffei L, Cremisi F (August 1994). "Developmental expression of PC3 gene is correlated with neuronal cell birthday" (PDF). Mechanisms of Development. 47 (2): 127–37. doi:10.1016/0925-4773(94)90085-X. PMID   7811636. S2CID   46597681. Archived from the original (PDF) on 2011-07-22.
  15. ↑ Iacopetti P, Michelini M, Stuckmann I, Oback B, Aaku-Saraste E, Huttner WB (April 1999). "Expression of the antiproliferative gene TIS21 at the onset of neurogenesis identifies single neuroepithelial cells that switch from proliferative to neuron-generating division". Proceedings of the National Academy of Sciences of the United States of America. 96 (8): 4639–44. Bibcode:1999PNAS...96.4639I. doi: 10.1073/pnas.96.8.4639 . PMC   16385 . PMID   10200315.
  16. ↑ Haubensak W, Attardo A, Denk W, Huttner WB (March 2004). "Neurons arise in the basal neuroepithelium of the early mammalian telencephalon: a major site of neurogenesis". Proceedings of the National Academy of Sciences of the United States of America. 101 (9): 3196–201. doi: 10.1073/pnas.0308600100 . PMC   365766 . PMID   14963232.
  17. ↑ Calegari F, Haubensak W, Haffner C, Huttner WB (July 2005). "Selective lengthening of the cell cycle in the neurogenic subpopulation of neural progenitor cells during mouse brain development". The Journal of Neuroscience. 25 (28): 6533–8. doi:10.1523/JNEUROSCI.0778-05.2005. PMC   6725437 . PMID   16014714.
  18. ↑ Götz M, Huttner WB (October 2005). "The cell biology of neurogenesis". Nature Reviews Molecular Cell Biology. 6 (10): 777–88. doi:10.1038/nrm1739. PMID   16314867. S2CID   16955231.
  19. 1 2 Kowalczyk, Tom; Pontious, Adria; Englund, Chris; Daza, Ray A. M.; Bedogni, Francesco; Hodge, Rebecca; Attardo, Alessio; Bell, Chris; Huttner, Wieland B. (2009-10-01). "Intermediate Neuronal Progenitors (Basal Progenitors) Produce Pyramidal–Projection Neurons for All Layers of Cerebral Cortex". Cerebral Cortex. 19 (10): 2439–2450. doi:10.1093/cercor/bhn260. ISSN   1047-3211. PMC   2742596 . PMID   19168665.
  20. 1 2 3 4 Canzoniere D, Farioli-Vecchioli S, Conti F, Ciotti MT, Tata AM, Augusti-Tocco G, Mattei E, Lakshmana MK, Krizhanovsky V, Reeves SA, Giovannoni R, Castano F, Servadio A, Ben-Arie N, Tirone F (March 2004). "Dual control of neurogenesis by PC3 through cell cycle inhibition and induction of Math1". The Journal of Neuroscience. 24 (13): 3355–69. doi:10.1523/JNEUROSCI.3860-03.2004. PMC   6730030 . PMID   15056715.
  21. 1 2 3 4 5 Farioli-Vecchioli S, Saraulli D, Costanzi M, Pacioni S, Cinà I, Aceti M, Micheli L, Bacci A, Cestari V, Tirone F (October 2008). "The timing of differentiation of adult hippocampal neurons is crucial for spatial memory". PLOS Biology. 6 (10): e246. doi:10.1371/journal.pbio.0060246. PMC   2561078 . PMID   18842068.
  22. ↑ Corrente G, Guardavaccaro D, Tirone F (March 2002). "PC3 potentiates NGF-induced differentiation and protects neurons from apoptosis" (PDF). NeuroReport. 13 (4): 417–22. doi:10.1097/00001756-200203250-00011. PMID   11930152. S2CID   4996878.
  23. ↑ el-Ghissassi F, Valsesia-Wittmann S, Falette N, Duriez C, Walden PD, Puisieux A (October 2002). "BTG2(TIS21/PC3) induces neuronal differentiation and prevents apoptosis of terminally differentiated PC12 cells". Oncogene. 21 (44): 6772–78. doi: 10.1038/sj.onc.1205888 . PMID   12360398.
  24. 1 2 3 4 5 6 Farioli-Vecchioli S, Saraulli D, Costanzi M, Leonardi L, Cinà I, Micheli L, Nutini M, Longone P, Oh SP, Cestari V, Tirone F (December 2009). "Impaired terminal differentiation of hippocampal granule neurons and defective contextual memory in PC3/Tis21 knockout mice". PLOS ONE. 4 (12): e8339. Bibcode:2009PLoSO...4.8339F. doi: 10.1371/journal.pone.0008339 . PMC   2791842 . PMID   20020054.
  25. ↑ Passeri D, Marcucci A, Rizzo G, Billi M, Panigada M, Leonardi L, Tirone F, Grignani F (July 2006). "Btg2 enhances retinoic acid-induced differentiation by modulating histone H4 methylation and acetylation". Molecular and Cellular Biology. 26 (13): 5023–32. doi:10.1128/MCB.01360-05. PMC   1489145 . PMID   16782888.
  26. 1 2 Lin WJ, Gary JD, Yang MC, Clarke S, Herschman HR (June 1996). "The mammalian immediate-early TIS21 protein and the leukemia-associated BTG1 protein interact with a protein-arginine N-methyltransferase". The Journal of Biological Chemistry. 271 (25): 15034–44. doi: 10.1074/jbc.271.25.15034 . PMID   8663146.
  27. ↑ Micheli L, Ceccarelli M, Farioli-Vecchioli S, Tirone F (December 2015). "Control of the Normal and Pathological Development of Neural Stem and Progenitor Cells by the PC3/Tis21/Btg2 and Btg1 Genes" (PDF). Journal of Cellular Physiology. 230 (12): 2881–90. doi:10.1002/jcp.25038. PMID   25967096. S2CID   206054527.
  28. ↑ Ceccarelli M, Micheli L, D'Andrea G, De Bardi M, Scheijen B, Ciotti M, Leonardi L, Luvisetto S, Tirone F (December 2015). "Altered cerebellum development and impaired motor coordination in mice lacking the Btg1 gene: Involvement of cyclin D1" (PDF). Developmental Biology. 408 (1): 109–25. doi: 10.1016/j.ydbio.2015.10.007 . PMID   26524254.
  29. ↑ Farioli-Vecchioli S, Micheli L, Saraulli D, Ceccarelli M, Cannas S, Scardigli R, Leonardi L, Cinà I, Costanzi M, Ciotti MT, Moreira P, Rouault JP, Cestari V, Tirone F (2012). "Btg1 is Required to Maintain the Pool of Stem and Progenitor Cells of the Dentate Gyrus and Subventricular Zone". Frontiers in Neuroscience. 6: 124. doi: 10.3389/fnins.2012.00124 . PMC   3431174 . PMID   22969701.
  30. ↑ Tirone F, Farioli-Vecchioli S, Micheli L, Ceccarelli M, Leonardi L (2013). "Genetic control of adult neurogenesis: interplay of differentiation, proliferation and survival modulates new neurons function, and memory circuits". Frontiers in Cellular Neuroscience. 7: 59. doi: 10.3389/fncel.2013.00059 . PMC   3653098 . PMID   23734097.
  31. ↑ Ceccarelli M, Micheli L, D'Andrea G, De Bardi M, Scheijen B, Ciotti M, Leonardi L, Luvisetto S, Tirone F (December 2015). "Altered cerebellum development and impaired motor coordination in mice lacking the Btg1 gene: Involvement of cyclin D1". Developmental Biology. 408 (1): 109–25. doi: 10.1016/j.ydbio.2015.10.007 . PMID   26524254. http://www.inmm.cnr.it/tirone/pdfs/Dev%20Biol%202015.pdf
  32. 1 2 Farioli-Vecchioli S, Cinà I, Ceccarelli M, Micheli L, Leonardi L, Ciotti MT, De Bardi M, Di Rocco C, Pallini R, Cavallaro S, Tirone F (October 2012). "Tis21 knock-out enhances the frequency of medulloblastoma in Patched1 heterozygous mice by inhibiting the Cxcl3-dependent migration of cerebellar neurons". The Journal of Neuroscience. 32 (44): 15547–64. doi:10.1523/JNEUROSCI.0412-12.2012. PMC   6621585 . PMID   23115191.
  33. 1 2 Ceccarelli M, Micheli L, Tirone F (2016). "Suppression of Medulloblastoma Lesions by Forced Migration of Preneoplastic Precursor Cells with Intracerebellar Administration of the Chemokine Cxcl3". Frontiers in Pharmacology. 7: 484. doi: 10.3389/fphar.2016.00484 . PMC   5159413 . PMID   28018222.
  34. ↑ Prévôt D, Voeltzel T, Birot AM, Morel AP, Rostan MC, Magaud JP, Corbo L (January 2000). "The leukemia-associated protein Btg1 and the p53-regulated protein Btg2 interact with the homeoprotein Hoxb9 and enhance its transcriptional activation". The Journal of Biological Chemistry. 275 (1): 147–53. doi: 10.1074/jbc.275.1.147 . PMID   10617598.
  35. ↑ Berthet C, Guéhenneux F, Revol V, Samarut C, Lukaszewicz A, Dehay C, Dumontet C, Magaud JP, Rouault JP (January 2002). "Interaction of PRMT1 with BTG/TOB proteins in cell signalling: molecular analysis and functional aspects". Genes to Cells. 7 (1): 29–39. doi: 10.1046/j.1356-9597.2001.00497.x . PMID   11856371.
  36. ↑ Prévôt D, Morel AP, Voeltzel T, Rostan MC, Rimokh R, Magaud JP, Corbo L (March 2001). "Relationships of the antiproliferative proteins BTG1 and BTG2 with CAF1, the human homolog of a component of the yeast CCR4 transcriptional complex: involvement in estrogen receptor alpha signaling pathway". The Journal of Biological Chemistry. 276 (13): 9640–8. doi: 10.1074/jbc.M008201200 . PMID   11136725.
  37. ↑ Micheli L, D'Andrea G, Leonardi L, Tirone F (2017). "HDAC1, HDAC4, and HDAC9 Bind to PC3/Tis21/Btg2 and Are Required for Its Inhibition of Cell Cycle Progression and Cyclin D1 Expression" (PDF). Journal of Cellular Physiology. 232 (7): 1696–1707. doi:10.1002/jcp.25467. PMID   27333946. S2CID   4070837.

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