SMAR1, a Novel, Alternatively Spliced Gene Product, Binds the Scaffold/Matrix-Associated Region at the T Cell Receptor β Locus

Chattopadhyay, Samit; Kaul, Ruchika; Charest, Alan; Housman, David E.; Chen, Jianzhu

doi:10.1006/geno.2000.6279

Cited by 57 publications

(73 citation statements)

References 15 publications

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“…Details of the V␤14 constructs are under "Experimental Procedures." MAR␤ alone contained only the 170-mer AT-rich sequence that binds to SMAR1 (32). No appreciable transcriptional activity was observed when the cells were transfected with either the control pGL2 vector or pGL2-MAR␤ either in the absence or in the presence of SMAR1 (Fig.…”

Section: Smar1 Acts As a Transcriptionalmentioning

confidence: 96%

“…SMAR1 Overexpression Mildly Perturbs T Cell Development at Early DN Stage-Earlier, we have shown that SMAR1 expression is higher during the DP stage compared with either the DN or SP stage T cells (32). We reasoned that overexpression of SMAR1 in transgenic mice may further elucidate its role in the T cell development.…”

Section: Smar1 Controls V(d)j Recombination and T Cell Developmentmentioning

confidence: 98%

“…32 and 33). During transition from DN to DP stage of thymocyte development, there is a halt in TCR␤ gene rearrangement at the DP stage during which MAR␤ is strongly induced, and a parallel upregulation in SMAR1 expression was observed (26,32). To investigate the role of SMAR1 in V(D)J recombination and T cell development, we generated SMAR1 transgenic mice using a eukaryotic expression vector carrying SMAR1 cDNA as described under "Experimental Procedures" (Fig.…”

Section: Analysis Of the Transgene In Mice Expressing Smar1-pre-mentioning

confidence: 99%

“…Mice-SMAR1 is highly expressed in DP thymocytes (32), and thus, it is possible that its binding to MAR␤ (induced during DN to DP transition) might control the V(D)J recombination at the TCR␤ locus in a stage-specific manner. Because overexpression of SMAR1 results in decreased population of mature T cells, T lymphocytes from thymus and lymph nodes were subjected to surface staining with a panel of V␤-specific antibodies using mouse V␤ TCR screening panel (BD PharMingen).…”

Section: Altered Frequency Of T Cells Expressing Specific V␤s In Tranmentioning

confidence: 99%

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Abnormal V(D)J Recombination of T Cell Receptor β Locus in SMAR1 Transgenic Mice

Kaul-Ghanekar

Majumdar

Jalota

et al. 2005

Journal of Biological Chemistry

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The immunoglobulin (Ig) and T cell receptor (TCR) 1 genes are assembled by a complex process of V(D)J recombination to generate antigen receptor diversity. In this process, the antigen binding domains of Ig and TCR chains that are encoded by germline variable (V), diversity (D), and joining (J) gene segments are rearranged to produce functional B or T cell receptors (1-3). For IgH and TCR␤ chains, V, D, and J gene segments are involved whereas for IgL and TCR␣ chains, V and J gene segments take part in the recombination event (4 -6). V(D)J recombination is known to be stage-specific within a given lymphoid lineage, and the antigen receptors are expressed from only one of the two alleles; the phenomenon called allelic exclusion (7,8). At the TCR␤ locus, the recombination occurs during DN (CD4 Ϫ CD8 Ϫ CD44 Ϫ CD25 ϩ ) stage of thymocyte development (9). V(D)J recombination is mediated by lymphoid and non-lymphoid-specific factors as well as cis regulatory elements (10). The lymphoid-specific factors of the recombination machinery include recombination activating genes (RAG) 1 and 2, and terminal deoxynucleotidyltransferase (TdT) (6, 10, and 11). Besides lymphoid-specific factors, nonlymphoid-restricted factors have also been implicated in the regulation of the recombination process. Among these, proteins that are involved in DNA double-strand break repair also play a critical role in the recombination events. These include Ku-80, XRCC4 protein, the catalytic subunit of DNA-dependent protein kinase (DNA-PK), and poly(ADP-ribose) polymerase (PARP) (12)(13)(14).

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Section: Smar1 Acts As a Transcriptionalmentioning

confidence: 96%

Section: Smar1 Controls V(d)j Recombination and T Cell Developmentmentioning

confidence: 98%

Section: Analysis Of the Transgene In Mice Expressing Smar1-pre-mentioning

confidence: 99%

Section: Altered Frequency Of T Cells Expressing Specific V␤s In Tranmentioning

confidence: 99%

See 2 more Smart Citations

Abnormal V(D)J Recombination of T Cell Receptor β Locus in SMAR1 Transgenic Mice

Kaul-Ghanekar

Majumdar

Jalota

et al. 2005

Journal of Biological Chemistry

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“…4B). These apparently opposing results in fact tempted us to hypothesize that SMAR1, being a well known transcriptional repressor of different genes (23), might inhibit Slug expression in wild type cells by binding to the MARs at Slug promoter locus thereby repressing its transcription, while in synthetic Slug cDNA-transfected cells, SMAR1 is failing to bind to Slug promoter locus due to the change in their …”

Section: Smar1 Regulates E-cadherin Transcription By Modulating the Ementioning

confidence: 99%

Inhibition of Epithelial to Mesenchymal Transition by E-cadherin Up-regulation via Repression of Slug Transcription and Inhibition of E-cadherin Degradation

Adhikary

Chakraborty

Mazumdar

et al. 2014

Journal of Biological Chemistry

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Background: Epithelial-mesenchymal transition (EMT) is an important program in tumor metastasis. Results: SMAR1 inhibits EMT by up-regulating E-cadherin in a dual manner via repression of Slug transcription and inhibition of E-cadherin degradation. Conclusion: SMAR1 functions as a critical protein in regulating EMT. Significance: This study provides a potential mechanism for the contribution of SMAR1 in inhibiting breast cancer metastasis.

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Direct interaction with and activation of p53 by SMAR1 retards cell‐cycle progression at G₂/M phase and delays tumor growth in mice

Kaul

Mukherjee

Ahmed

et al. 2002

Intl Journal of Cancer

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The tumor-suppressor p53 is a multifunctional protein mainly responsible for maintaining genomic integrity. p53 induces its tumor-suppressor activity by either causing cellcycle arrest (G 1 /S or G 2 /M) or inducing cells to undergo apoptosis. This function of wild-type p53 as "guardian of the genome" is presumably achieved by forming molecular complexes with different DNA targets as well as by interacting with a number of cellular proteins, e.g., Mdm2, Gadd45, p21, 14-3-3, Bax and Apaf-1. Upon activation, p53 activates p21, which in turn controls the cell cycle by regulating G 1 or G 2 checkpoints. Here, we report SMAR1 as one such p53-interacting protein that is involved in delaying tumor progression in vivo as well as in regulating the cell cycle. SMAR1S activates p53-mediated reporter gene expression in mouse melanoma cells, breast cancer cells (MCF-7) and p53 null cells (K562), followed by activation of its downstream effector, p21. We further demonstrate that SMAR1 physically interacts and colocalizes with p53. These data together suggest that SMAR1 is the only known MARBP that delays tumor progression via direct activation and interaction with tumor-suppressor p53.

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SMAR1, a Novel, Alternatively Spliced Gene Product, Binds the Scaffold/Matrix-Associated Region at the T Cell Receptor β Locus

Cited by 57 publications

References 15 publications

Abnormal V(D)J Recombination of T Cell Receptor β Locus in SMAR1 Transgenic Mice

Abnormal V(D)J Recombination of T Cell Receptor β Locus in SMAR1 Transgenic Mice

Inhibition of Epithelial to Mesenchymal Transition by E-cadherin Up-regulation via Repression of Slug Transcription and Inhibition of E-cadherin Degradation

Direct interaction with and activation of p53 by SMAR1 retards cell‐cycle progression at G₂/M phase and delays tumor growth in mice

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SMAR1, a Novel, Alternatively Spliced Gene Product, Binds the Scaffold/Matrix-Associated Region at the T Cell Receptor β Locus

Cited by 57 publications

References 15 publications

Abnormal V(D)J Recombination of T Cell Receptor β Locus in SMAR1 Transgenic Mice

Abnormal V(D)J Recombination of T Cell Receptor β Locus in SMAR1 Transgenic Mice

Inhibition of Epithelial to Mesenchymal Transition by E-cadherin Up-regulation via Repression of Slug Transcription and Inhibition of E-cadherin Degradation

Direct interaction with and activation of p53 by SMAR1 retards cell‐cycle progression at G2/M phase and delays tumor growth in mice

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Direct interaction with and activation of p53 by SMAR1 retards cell‐cycle progression at G₂/M phase and delays tumor growth in mice