You Searched For: 7.2+CPG+[TQ7.2+CPG]

Catalog Number: (10103-478)

Supplier: Prosci

Description: CpG methylation is an epigenetic modification that is important for embryonic development, imprinting, and X-chromosome inactivation. Studies in mice have demonstrated that DNA methylation is required for mammalian development. TRDMT1 is a protein with similarity to DNA methyltransferases, but this protein does not display methyltransferase activity. The protein strongly binds DNA, suggesting that it may mark specific sequences in the genome.CpG methylation is an epigenetic modification that is important for embryonic development, imprinting, and X-chromosome inactivation. Studies in mice have demonstrated that DNA methylation is required for mammalian development. This gene encodes a protein with similarity to DNA methyltransferases, but this protein does not display methyltransferase activity. The protein strongly binds DNA, suggesting that it may mark specific sequences in the genome. Alternative splicing results in multiple transcript variants encoding different isoforms.

Catalog Number: (10487-476)

Supplier: Bioss

Description: P55 is an extensively palmitoylated erythrocyte membrane protein, and a member of the MAGUK family. P55 also resists salt extraction, resulting in a high affinity for the plasma membrane. P55 contains a PDZ/DHR domain, a conserved SH-3 domain that appears to suppress tyrosine kinase activity of various oncoproteins, a 39-amino acid motif that binds to cytoskeletal protein 4.1R, and a guanylate kinase-like domain. Interaction with glycophorin C (GPC) and 4.1R suggests that p55 may play a role in the dynamic regulation in the erythrocyte membrane. In addition, p55 gene expression in vivo may be associated with a CpG island. P55 is constitutively expressed in K562 erythroleukemia cells during erythropoiesis and undergoes a 2-fold amplification after induction.

Catalog Number: (10487-474)

Supplier: Bioss

Description: P55 is an extensively palmitoylated erythrocyte membrane protein, and a member of the MAGUK family. P55 also resists salt extraction, resulting in a high affinity for the plasma membrane. P55 contains a PDZ/DHR domain, a conserved SH-3 domain that appears to suppress tyrosine kinase activity of various oncoproteins, a 39-amino acid motif that binds to cytoskeletal protein 4.1R, and a guanylate kinase-like domain. Interaction with glycophorin C (GPC) and 4.1R suggests that p55 may play a role in the dynamic regulation in the erythrocyte membrane. In addition, p55 gene expression in vivo may be associated with a CpG island. P55 is constitutively expressed in K562 erythroleukemia cells during erythropoiesis and undergoes a 2-fold amplification after induction.

Supplier: Adipogen

Description: In recent years several groups have studied the sequence requirements, specificity, signaling pathways and kinetics of the TLR (Toll-like receptor) 9 suppression by inhibitory oligonucleotide motifs, which led to a class of novel inhibitory oligonucleotide (iODNs), that is independent of the previously thought species preference. Subsequently it has been discovered that telomeric DNA repeats (TTAGGG)n can block immune activation by CpG-ODNs. Short, 11-15 base long oligonucleotides were synthesized that were capable of potently inhibiting CpG-stimulation. The optimal inhibitory DNA motif consists of a pyrimidine-rich triplet, preferably CCT, which is positioned 5- to the GGG sequence in a singlestranded DNA molecule. Additionally, both the optimal spacing between the CCT and GGG motifs, as well as their relative order to each other, is of crucial importance for the inhibitory DNA action. Interestingly, although both TLR7/TLR8 ligands and bacterial DNA share the endosomal compartment for receptor binding and signal transduction, certain iODNs (G-type) suppress only TLR9-mediated activation, whereas prototype class I iODN may also interfere with the activation via the TLR7/TLR8 pathway. Recently, intriguing evidence has been presented that for some iODN classes the immuno-modulatory biological activity shows only limited sequence dependency or may not even involve TLR-mediated uptake and signaling pathways. For example iODNs of the class II are thought to act on immune activation through inhibition of STAT signaling and independent of TLR signaling via binding to a yet to be identified 'ODN-receptor'. Slightly modified phosphodiester versions of the most potent inhibitory ODNs were also able to profoundly block the immune activation of macrophages and just recently prove to be valuable tools for in vivo use in experimental animal models of inflammatory and auto-immune diseases. Based upon these recent insights the following classification for iODNs has been suggested: Class I: G-stretch ODNs: TLR9-specific competitors, some iODNs may also affect TLR7 and TLR8 signalingClass II: ODNs with telomeric repeats: TLR-independent inhibitors of STAT signaling (cellular uptake via an 'ODN receptor'?)Class III: Inhibitors of DNA uptake in a sequence independent mannerClass IV: Long phosphorothioate ODNs as direct competitors of TLR9 signaling in a sequence independent manner

Catalog Number: (76120-610)

Supplier: Bioss

Description: Frequent loss of heterozygosity (LOH) at human chromosome 8p22-p21 is associated with various tumors including prostate and breast cancer. The 8p22-p21 region contains the FEZ1 gene, which is altered in tumors of the esophagus, prostate and breast. The FEZ1 protein (also known as leucine zipper putative tumor suppressor or LZTS1) contains a DNA-binding leucine zipper motif. FEZ1 is expressed in normal breast and prostate, but alterations in FEZ1 expression result in abnormal cell growth. The absence of FEZ1 expression is characteristic of breast and prostate cancer cell lines as well as primary breast and pro-state tumors. This absence of FEZ1 may be due to several factors, including mutations in the FEZ1 gene or hypermethylation of the CpG island flanking the FEZ1 promoter region. FEZ1 acts as a negative regulator of cell growth. During cell-cycle progression, FEZ1 localizes to microtubule components and is hyperphosphorylated by cAMP-dependent kinase.

Catalog Number: (CAPIPA5-18619)

Supplier: Thermo Scientific

Description: This antibody is predicted to react with canine, mouse and rat based on sequence homology. DNA methylation is the major modification of eukaryotic genomes and plays an essential role in mammalian development. Human proteins MECP2, MBD1, MBD2, MBD3, and MBD4 comprise a family of nuclear proteins related by the presence in each of a methyl-CpG binding domain . Each of these proteins, with the exception of MBD3, is capable of binding specifically to methylated DNA. MECP2, MBD1 and MBD2 can also repress transcription from methylated gene promoters. The protein encoded by this gene may function as a mediator of the biological consequences of the methylation signal. It is also reported that the this protein functions as a demethylase to activate transcription, as DNA methylation causes gene silencing. Two transcript variants encoding different isoforms have been found for this gene.

Supplier: Adipogen

Description: In recent years several groups have studied the sequence requirements, specificity, signaling pathways and kinetics of the TLR (Toll-like receptor) 9 suppression by inhibitory oligonucleotide motifs, which led to a class of novel inhibitory oligonucleotide (iODNs), that is independent of the previously thought species preference. Subsequently it has been discovered that telomeric DNA repeats (TTAGGG)n can block immune activation by CpG-ODNs. Short, 11-15 base long oligonucleotides were synthesized that were capable of potently inhibiting CpG-stimulation. The optimal inhibitory DNA motif consists of a pyrimidine-rich triplet, preferably CCT, which is positioned 5- to the GGG sequence in a singlestranded DNA molecule. Additionally, both the optimal spacing between the CCT and GGG motifs, as well as their relative order to each other, is of crucial importance for the inhibitory DNA action. Interestingly, although both TLR7/TLR8 ligands and bacterial DNA share the endosomal compartment for receptor binding and signal transduction, certain iODNs (G-type) suppress only TLR9-mediated activation, whereas prototype class I iODN may also interfere with the activation via the TLR7/TLR8 pathway. Recently, intriguing evidence has been presented that for some iODN classes the immuno-modulatory biological activity shows only limited sequence dependency or may not even involve TLR-mediated uptake and signaling pathways. For example iODNs of the class II are thought to act on immune activation through inhibition of STAT signaling and independent of TLR signaling via binding to a yet to be identified 'ODN-receptor'. Slightly modified phosphodiester versions of the most potent inhibitory ODNs were also able to profoundly block the immune activation of macrophages and just recently prove to be valuable tools for in vivo use in experimental animal models of inflammatory and auto-immune diseases. Based upon these recent insights the following classification for iODNs has been suggested: Class I: G-stretch ODNs: TLR9-specific competitors, some iODNs may also affect TLR7 and TLR8 signalingClass II: ODNs with telomeric repeats: TLR-independent inhibitors of STAT signaling (cellular uptake via an 'ODN receptor'?)Class III: Inhibitors of DNA uptake in a sequence independent mannerClass IV: Long phosphorothioate ODNs as direct competitors of TLR9 signaling in a sequence independent manner

Supplier: Adipogen

Description: In recent years several groups have studied the sequence requirements, specificity, signaling pathways and kinetics of the TLR (Toll-like receptor) 9 suppression by inhibitory oligonucleotide motifs, which led to a class of novel inhibitory oligonucleotide (iODNs), that is independent of the previously thought species preference. Subsequently it has been discovered that telomeric DNA repeats (TTAGGG)n can block immune activation by CpG-ODNs. Short, 11-15 base long oligonucleotides were synthesized that were capable of potently inhibiting CpG-stimulation. The optimal inhibitory DNA motif consists of a pyrimidine-rich triplet, preferably CCT, which is positioned 5- to the GGG sequence in a singlestranded DNA molecule. Additionally, both the optimal spacing between the CCT and GGG motifs, as well as their relative order to each other, is of crucial importance for the inhibitory DNA action. Interestingly, although both TLR7/TLR8 ligands and bacterial DNA share the endosomal compartment for receptor binding and signal transduction, certain iODNs (G-type) suppress only TLR9-mediated activation, whereas prototype class I iODN may also interfere with the activation via the TLR7/TLR8 pathway. Recently, intriguing evidence has been presented that for some iODN classes the immuno-modulatory biological activity shows only limited sequence dependency or may not even involve TLR-mediated uptake and signaling pathways. For example iODNs of the class II are thought to act on immune activation through inhibition of STAT signaling and independent of TLR signaling via binding to a yet to be identified 'ODN-receptor'. Slightly modified phosphodiester versions of the most potent inhibitory ODNs were also able to profoundly block the immune activation of macrophages and just recently prove to be valuable tools for in vivo use in experimental animal models of inflammatory and auto-immune diseases. Based upon these recent insights the following classification for iODNs has been suggested: Class I: G-stretch ODNs: TLR9-specific competitors, some iODNs may also affect TLR7 and TLR8 signalingClass II: ODNs with telomeric repeats: TLR-independent inhibitors of STAT signaling (cellular uptake via an 'ODN receptor'?)Class III: Inhibitors of DNA uptake in a sequence independent mannerClass IV: Long phosphorothioate ODNs as direct competitors of TLR9 signaling in a sequence independent manner

Catalog Number: (89359-894)

Supplier: Genetex

Description: Methylation of DNA at cytosine residues plays an important role in regulation of gene expression, genomic imprinting and is essential for mammalian development. Hypermethylation of CpG islands in tumor suppressor genes or hypomethylation of bulk genomic DNA may be linked with development of cancer. To date, 3 families of mammalian DNA methyltransferase genes have been identified which include Dnmt1, Dnmt2 and Dnmt3. Dnmt1 is constitutively expressed in proliferating cells and inactivation of this gene causes global demethylation of genomic DNA and embryonic lethality. Dnmt2 is expressed at low levels in adult tissues and its inactivation does not affect DNA methylation or maintenance of methylation. The Dnmt3 family members, Dnmt3a and Dnmt3b, are strongly expressed in ES cells but their expression is down regulated in differentiating ES cells and is low in adult somatic tissue. Dnmt1 co-purifies with the retinoblastoma (Rb) tumour suppressor gene product, E2F1, and HDAC1. Dnmt1 also cooperates with Rb to repress transcription from promoters containing E2Fbinding sites suggesting a link between DNA methylation, histone deacetylase and sequence-specific DNA binding activity, as well as a growth-regulatory pathway that is disrupted in nearly all cancer cells.

Catalog Number: (10751-194)

Supplier: Prosci

Description: ZBTB4 Antibody: The ZBTB family of proteins is comprised of diverse zinc finger proteins that also contain a BTB (BR-C, ttk and bab) domain. Similar to Kaiso, a zinc-finger containing protein that can bind methylated CpGs, ZBTB4 can also bind methylated DNA and repress transcription. ZBTB4 has been shown to associate with the Sin3/histone deacetylase co-repressor and repress expression of P21CIP1 as part of a heterodimeric complex with Miz1. In cultured cells, depletion of ZBTB4 promotes cell cycle arrest in response to p53 activation and suppresses apoptosis through regulation of P21CIP1, suggesting that ZBTB4 is a critical determinant of the cellular response to p53 activation. HIPK2, a kinase that is involved in cellular proliferation and survival, phosphorylates and down-regulates ZBTB4 under normal cell growth conditions; this degradation increases with DNA damage.

Catalog Number: (77439-296)

Supplier: Bioss

Description: The tumor suppressor gene RASSF1A (3p21.3), human Ras association domain family 1A, is expressed in heart, brain, placenta, lung, liver, skeletal muscle, kidney, pancreas, spleen, thymus, prostate, testis, small intestine, colon, and peripheral blood leukocytes. RASSF1A expression is inhibited by hypermethylation of the CpG island including the promoter and early transcribed regions of the human RASSF1A gene. Hypermethylated RASSF1A promoter is observed in primary tumors. Furthermore, RASSF1A is related with cell cycle regulation, apoptosis and microtubule stability. Potential tumor suppressor. Isoform A interacts with CDC20, an activator of the anaphase-promoting complex, APC, resulting in the inhibition of APC activity and mitotic progression. More specifically, RASSF1a inhibits proliferation by negatively regulating cell cycle progression at the level of G1/S-phase transition by regulating accumulation of cyclin D1 protein. It also inhibits the activation of STK3 and STK4 and may play an additional role as a scaffold protein, directing these enzymes to sites of activation. Isoform C has been shown not to perform these roles, and no function has been identified for this isoform.

Catalog Number: (10496-156)

Supplier: Bioss

Description: Frequent loss of heterozygosity (LOH) at human chromosome 8p22-p21 is associated with various tumors including prostate and breast cancer. The 8p22-p21 region contains the FEZ1 gene, which is altered in tumors of the esophagus, prostate and breast. The FEZ1 protein (also known as leucine zipper putative tumor suppressor or LZTS1) contains a DNA-binding leucine zipper motif. FEZ1 is expressed in normal breast and prostate, but alterations in FEZ1 expression result in abnormal cell growth. The absence of FEZ1 expression is characteristic of breast and prostate cancer cell lines as well as primary breast and pro-state tumors. This absence of FEZ1 may be due to several factors, including mutations in the FEZ1 gene or hypermethylation of the CpG island flanking the FEZ1 promoter region. FEZ1 acts as a negative regulator of cell growth. During cell-cycle progression, FEZ1 localizes to microtubule components and is hyperphosphorylated by cAMP-dependent kinase.

Catalog Number: (10496-094)

Supplier: Bioss

Description: Frequent loss of heterozygosity (LOH) at human chromosome 8p22-p21 is associated with various tumors including prostate and breast cancer. The 8p22-p21 region contains the FEZ1 gene, which is altered in tumors of the esophagus, prostate and breast. The FEZ1 protein (also known as leucine zipper putative tumor suppressor or LZTS1) contains a DNA-binding leucine zipper motif. FEZ1 is expressed in normal breast and prostate, but alterations in FEZ1 expression result in abnormal cell growth. The absence of FEZ1 expression is characteristic of breast and prostate cancer cell lines as well as primary breast and pro-state tumors. This absence of FEZ1 may be due to several factors, including mutations in the FEZ1 gene or hypermethylation of the CpG island flanking the FEZ1 promoter region. FEZ1 acts as a negative regulator of cell growth. During cell-cycle progression, FEZ1 localizes to microtubule components and is hyperphosphorylated by cAMP-dependent kinase.

Catalog Number: (89367-210)

Supplier: Genetex

Description: Methylation of DNA at cytosine residues plays an important role in regulation of gene expression, genomic imprinting and is essential for mammalian development. Hypermethylation of CpG islands in tumor suppressor genes or hypomethylation of bulk genomic DNA may be linked with development of cancer. To date, 3 families of mammalian DNA methyltransferase genes have been identified which include Dnmt1, Dnmt2 and Dnmt3. Dnmt1 is constitutively expressed in proliferating cells and inactivation of this gene causes global demethylation of genomic DNA and embryonic lethality. Dnmt2 is expressed at low levels in adult tissues and its inactivation does not affect DNA methylation or maintenance of methylation. The Dnmt3 family members, Dnmt3a and Dnmt3b, are strongly expressed in ES cells but their expression is down regulated in differentiating ES cells and is low in adult somatic tissue. Dnmt 1 co-purifies with the retinoblastoma (Rb) tumour suppressor gene product, E2F1, and HDAC1. Dnmt 1 also cooperates with Rb to repress transcription from promoters containing E2F binding sites suggesting a link between DNA methylation, histone deacetylase and sequence-specific DNA binding activity, as well as a growth-regulatory pathway that is disrupted in nearly all cancer cells.

Catalog Number: (102981-408)

Supplier: Adipogen

Description: In recent years several groups have studied the sequence requirements, specificity, signaling pathways and kinetics of the TLR (Toll-like receptor) 9 suppression by inhibitory oligonucleotide motifs, which led to a class of novel inhibitory oligonucleotide (iODNs), that is independent of the previously thought species preference. Subsequently it has been discovered that telomeric DNA repeats (TTAGGG)n can block immune activation by CpG-ODNs. Short, 11-15 base long oligonucleotides were synthesized that were capable of potently inhibiting CpG-stimulation. The optimal inhibitory DNA motif consists of a pyrimidine-rich triplet, preferably CCT, which is positioned 5- to the GGG sequence in a singlestranded DNA molecule. Additionally, both the optimal spacing between the CCT and GGG motifs, as well as their relative order to each other, is of crucial importance for the inhibitory DNA action. Interestingly, although both TLR7/TLR8 ligands and bacterial DNA share the endosomal compartment for receptor binding and signal transduction, certain iODNs (G-type) suppress only TLR9-mediated activation, whereas prototype class I iODN may also interfere with the activation via the TLR7/TLR8 pathway. Recently, intriguing evidence has been presented that for some iODN classes the immuno-modulatory biological activity shows only limited sequence dependency or may not even involve TLR-mediated uptake and signaling pathways. For example iODNs of the class II are thought to act on immune activation through inhibition of STAT signaling and independent of TLR signaling via binding to a yet to be identified 'ODN-receptor'. Slightly modified phosphodiester versions of the most potent inhibitory ODNs were also able to profoundly block the immune activation of macrophages and just recently prove to be valuable tools for in vivo use in experimental animal models of inflammatory and auto-immune diseases. Based upon these recent insights the following classification for iODNs has been suggested: Class I: G-stretch ODNs: TLR9-specific competitors, some iODNs may also affect TLR7 and TLR8 signalingClass II: ODNs with telomeric repeats: TLR-independent inhibitors of STAT signaling (cellular uptake via an 'ODN receptor'?)Class III: Inhibitors of DNA uptake in a sequence independent mannerClass IV: Long phosphorothioate ODNs as direct competitors of TLR9 signaling in a sequence independent manner

Catalog Number: (76120-612)

Supplier: Bioss

Description: Frequent loss of heterozygosity (LOH) at human chromosome 8p22-p21 is associated with various tumors including prostate and breast cancer. The 8p22-p21 region contains the FEZ1 gene, which is altered in tumors of the esophagus, prostate and breast. The FEZ1 protein (also known as leucine zipper putative tumor suppressor or LZTS1) contains a DNA-binding leucine zipper motif. FEZ1 is expressed in normal breast and prostate, but alterations in FEZ1 expression result in abnormal cell growth. The absence of FEZ1 expression is characteristic of breast and prostate cancer cell lines as well as primary breast and pro-state tumors. This absence of FEZ1 may be due to several factors, including mutations in the FEZ1 gene or hypermethylation of the CpG island flanking the FEZ1 promoter region. FEZ1 acts as a negative regulator of cell growth. During cell-cycle progression, FEZ1 localizes to microtubule components and is hyperphosphorylated by cAMP-dependent kinase.