1083 Results for: "Tide+Quencher\\\\\\\\u2122+2+CPG"

Supplier: Bioss

Facilitator of innate immune signaling that promotes the production of type I interferon (IFN-alpha and IFN-beta). Innate immune response is triggered in response to non-CpG double-stranded DNA from viruses and bacteria delivered to the cytoplasm. Able to activate both NF-kappa-B and IRF3 transcription pathways to induce expression of type I interferon and exert a potent anti-viral state following expression. May be involved in translocon function, the translocon possibly being able to influence the induction of type I interferons. May be involved in transduction of apoptotic signals via its association with the major histocompatibility complex class II (MHC-II). Mediates death signaling via activation of the extracellular signal-regulated kinase (ERK) pathway.

Supplier: Bioss

Facilitator of innate immune signaling that promotes the production of type I interferon (IFN-alpha and IFN-beta). Innate immune response is triggered in response to non-CpG double-stranded DNA from viruses and bacteria delivered to the cytoplasm. Able to activate both NF-kappa-B and IRF3 transcription pathways to induce expression of type I interferon and exert a potent anti-viral state following expression. May be involved in translocon function, the translocon possibly being able to influence the induction of type I interferons. May be involved in transduction of apoptotic signals via its association with the major histocompatibility complex class II (MHC-II). Mediates death signaling via activation of the extracellular signal-regulated kinase (ERK) pathway.

Supplier: Bioss

Facilitator of innate immune signaling that promotes the production of type I interferon (IFN-alpha and IFN-beta). Innate immune response is triggered in response to non-CpG double-stranded DNA from viruses and bacteria delivered to the cytoplasm. Able to activate both NF-kappa-B and IRF3 transcription pathways to induce expression of type I interferon and exert a potent anti-viral state following expression. May be involved in translocon function, the translocon possibly being able to influence the induction of type I interferons. May be involved in transduction of apoptotic signals via its association with the major histocompatibility complex class II (MHC-II). Mediates death signaling via activation of the extracellular signal-regulated kinase (ERK) pathway.

Supplier: ProSci Inc.

PLEKHM3 Antibody: PLEKHM3, also known as DAPR, is a member of the M family of Pleckstrin homology domain-containing proteins. PLEKHM3 was initially identified through chromatin immunoprecipitation and CpG microarray analysis examining proteins regulated by myocyte-enhancing factor 2. In C2C12 myoblast cells, PLEKHM3 binds to the PI3K signaling member protein kinase B in the cytosol prior to differentiation into myotubes. Following the initiation of differentiation, PLEKHM3 was also found in membrane fractions. Knockdown of PLEKHM3 expression by RNAi resulted in the inhibition of myotube formation, suggesting that PLEKHM3 is a key component required by myoblasts for orchestrating their differentiation during myogenesis.

Supplier: Bioss

Facilitator of innate immune signaling that promotes the production of type I interferon (IFN-alpha and IFN-beta). Innate immune response is triggered in response to non-CpG double-stranded DNA from viruses and bacteria delivered to the cytoplasm. Able to activate both NF-kappa-B and IRF3 transcription pathways to induce expression of type I interferon and exert a potent anti-viral state following expression. May be involved in translocon function, the translocon possibly being able to influence the induction of type I interferons. May be involved in transduction of apoptotic signals via its association with the major histocompatibility complex class II (MHC-II). Mediates death signaling via activation of the extracellular signal-regulated kinase (ERK) pathway.

Supplier: Biotium

This MAb recognizes the HLA-B27 cell surface antigen on human cells. It may be used to HLA type human lymphocytes. Approximately 60% of patients with ankylosing spondylitis are HLA-B27 positive. This reagent can be used to help identify this HLA haplotype in human lymphocytes. Major histocompatibility complex (MHC) molecules form an integral part of the immune response system. They are cell-surface receptors that bind pep- tides and present them to T lymphocytes. Human leukocyte antigens (HLAs) are polymorphic members of the MHC family that are specifically involved in the presentation of antigens to the T cell receptor. There are two classes of HLA antigens: class I (HLA-A, HLA-B and HLA-C) and class II (HLA-D). Class I molecules are expressed in nearly all cells and play a central role in the immune system by presenting peptides derived from the endoplasmic reticulum. The differential structural properties of MHC class I and class II molecules account for their respective roles in activating different populations of T lymphocytes. HLA-B encodes a membrane anchored heavy chain, which hetero-dimerizes with a light chain (beta-2-Microglobulin) to form MHC-I. Polymorphisms yield hundreds of HLA-B alleles. The HLA-B27 allele appears with increased frequency in uveitis patients.

Supplier: ProSci Inc.

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 (MBD). 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. In contrast to other MBD family members, MECP2 is X-linked and subject to X inactivation. MECP2 is dispensible in stem cells, but is essential for embryonic development. MECP2 gene mutations are the cause of some cases of Rett syndrome, a progressive neurologic developmental disorder and one of the most common causes of mental retardation in females.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 (MBD). 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. In contrast to other MBD family members, MECP2 is X-linked and subject to X inactivation. MECP2 is dispensible in stem cells, but is essential for embryonic development. MECP2 gene mutations are the cause of some cases of Rett syndrome, a progressive neurologic developmental disorder and one of the most common causes of mental retardation in females.

Supplier: ProSci Inc.

TLR9 Antibody: Toll-like receptors (TLRs) are evolutionarily conserved pattern-recognition molecules resembling the toll proteins that mediate antimicrobial responses in Drosophila. These proteins recognize different microbial products during infection and serve as an important link between the innate and adaptive immune responses. TLR9 forms a subfamily along with TLR7 and TLR8 that recognize viral RNA and CpG DNA sequences and are localized in intracellular acidic compartments such as the phagolysosome. Unlike other TLRs which act through adaptor molecules such as TOLLIP, TIRAP, TRIF, and MyD88 to activate various kinases and transcription factors to respond to potential infection, TLR9 is strictly dependent on MyD88.

Supplier: ProSci Inc.

TLR9 Antibody: Toll-like receptors (TLRs) are evolutionarily conserved pattern-recognition molecules resembling the toll proteins that mediate antimicrobial responses in Drosophila. These proteins recognize different microbial products during infection and serve as an important link between the innate and adaptive immune responses. TLR9 forms a subfamily along with TLR7 and TLR8 that recognize viral RNA and CpG DNA sequences and are localized in intracellular acidic compartments such as the phagolysosome. Unlike other TLRs which act through adaptor molecules such as TOLLIP, TIRAP, TRIF, and MyD88 to activate various kinases and transcription factors to respond to potential infection, TLR9 is strictly dependent on MyD88.

Supplier: ProSci Inc.

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 (MBD). 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.

Supplier: ProSci Inc.

PRTFDC1 Antibody: Phosphoribosyl transferase domain containing 1 (PRTFDC1) is highly homologous to the hypoxanthine phosphoribosyltransferase (HPRT1) and may have arisen from a gene duplication event of a common ancestor gene. Recently, it was shown that CpG islands in the PRTFDC1 promoter could be hypermethylated in ovarian cancers and oral squamous-cell carcinomas (OSCC), leading to gene silencing. Restoration of PRTFDC1 expression in OSCC inhibited cell growth in colony-formation assays, while knockdown of PRTFDC1 expression in OSCC that expressed the gene promoted cell growth. These results suggest that PRTFDC1 can act as a tumor-suppressor gene. At least three isoforms of PRTFDC1 are known to exist.

Supplier: ProSci Inc.

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 (MBD). However, unlike the other family members, MBD3 is not capable of binding to methylated DNA. The predicted MBD3 protein shares 71% and 94% identity with MBD2 (isoform 1) and mouse Mbd3. MBD3 is a subunit of the NuRD, a multisubunit complex containing nucleosome remodeling and histone deacetylase activities. MBD3 mediates the association of metastasis-associated protein 2 (MTA2) with the core histone deacetylase complex.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 (MBD). However, unlike the other family members, MBD3 is not capable of binding to methylated DNA. The predicted MBD3 protein shares 71% and 94% identity with MBD2 (isoform 1) and mouse Mbd3. MBD3 is a subunit of the NuRD, a multisubunit complex containing nucleosome remodeling and histone deacetylase activities. MBD3 mediates the association of metastasis-associated protein 2 (MTA2) with the core histone deacetylase complex. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Entrez Gene record to access additional publications.

Supplier: Biotium

This MAb recognizes the HLA-B27 cell surface antigen on human cells. It may be used to HLA type human lymphocytes. Approximately 60% of patients with ankylosing spondylitis are HLA-B27 positive. This reagent can be used to help identify this HLA haplotype in human lymphocytes. Major histocompatibility complex (MHC) molecules form an integral part of the immune response system. They are cell-surface receptors that bind pep- tides and present them to T lymphocytes. Human leukocyte antigens (HLAs) are polymorphic members of the MHC family that are specifically involved in the presentation of antigens to the T cell receptor. There are two classes of HLA antigens: class I (HLA-A, HLA-B and HLA-C) and class II (HLA-D). Class I molecules are expressed in nearly all cells and play a central role in the immune system by presenting peptides derived from the endoplasmic reticulum. The differential structural properties of MHC class I and class II molecules account for their respective roles in activating different populations of T lymphocytes. HLA-B encodes a membrane anchored heavy chain, which hetero-dimerizes with a light chain (beta-2-Microglobulin) to form MHC-I. Polymorphisms yield hundreds of HLA-B alleles. The HLA-B27 allele appears with increased frequency in uveitis patients.

Supplier: ProSci Inc.

ECRG4 Antibody: The esophageal cancer-related gene 4 (ECRG4), also known as Augurin, was identified through differential display screening between esophageal cancer and normal tissue. Hypermethylation of CpG sites in the ECRG4 promoter correlate with ECRG4 downregulation in numerous esophageal squamous cell carcinoma tissues.. In transfected cells, overexpression of ECRG4 induced G1 arrest, dephosphorylation of Rb and decreased expression of cyclins D1 and D3. Increased expression of ECRG4 in aged mouse brain is observed compared with young mouse brain. The increased ECRG4 level was accompanied by elevated senescence-associated acidic beta-galactosidase activity, suggesting that ECRG4 is involved in cellular differentiation and senescence.

Supplier: Bioss

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.

Supplier: Bioss

Fragile X syndrome is the most frequent form of inherited mental retardation and is the result of transcriptional silencing of the FMR1 gene on the X chromosome. The FMR1 gene contains a distinct CpG dinucleotide repeat located in the 5' untranslated region of the gene. In fragile X syndrome this tandem repeat is substantially amplified and subjected to extensive methylation and enhanced transcriptional silencing. The FMR1 protein (or FMRP) is an RNA-binding protein that associates with polyribosomes and is a likely component of a messenger ribonuclear protein (mRNP) particle. It contains several features that are characteristics of RNA-binding proteins, including two hnRNPK homology (KH) domains and an RGG amino acid motif (RGG box). FMR1 localizes to both the nucleus and the cytoplasm and can also interact with two fragile X syndrome related factors, FXR1 and FXR2, which form heterodimers through their N-terminal coiled-coil domains. Since FMR1 contains both a nuclear localization signal and a nuclear export signal it is also implicated in the nucleocytoplasmic transport of mRNAs.

Supplier: Bioss

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.

Supplier: Bioss

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.

Supplier: Bioss

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.

Supplier: Bioss

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.

Supplier: Bioss

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.

Supplier: Bioss

Frequent loss of heterozygosity (LOH) at human chromosome 8p22-p21 is associated with various tumours including prostate and breast cancer. The 8p22-p21 region contains the FEZ1 gene, which is altered in tumours of the esophagus, prostate and breast. The FEZ1 protein (also known as leucine zipper putative tumour 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 tumours. 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.

Supplier: Bioss

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.

Supplier: Bioss

Frequent loss of heterozygosity (LOH) at human chromosome 8p22-p21 is associated with various tumours including prostate and breast cancer. The 8p22-p21 region contains the FEZ1 gene, which is altered in tumours of the esophagus, prostate and breast. The FEZ1 protein (also known as leucine zipper putative tumour 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 tumours. 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.

Supplier: Bioss

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.

Supplier: ProSci Inc.

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 nuclear protein with similarity to DNA methyltransferases. This protein is not thought to function as a DNA methyltransferase as it does not contain the amino acid residues necessary for methyltransferase activity. However, this protein does stimulate de novo methylation by DNA cytosine methyltransferase 3 alpha and it is thought to be required for the establishment of maternal genomic imprints. This protein also mediates transcriptional repression through interaction with histone deacetylase 1. Alternative splicing results in two transcript variants. An additional splice variant has been described but its biological validity has not been determined.

Supplier: Bioss

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.

Supplier: Bioss

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.

Supplier: Bioss

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.

Supplier: ProSci Inc.

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.