15220 Results for: "4-Formylphenyl-beta-D-allofuranose"

Supplier: Prosci

HSD17B6 has both oxidoreductase and epimerase activities and is involved in androgen catabolism. The oxidoreductase activity can convert 3 alpha-adiol to dihydrotestosterone, while the epimerase activity can convert androsterone to epi-androsterone. Both reactions use NAD+ as the preferred cofactor. HSD17B6 is a member of the retinol dehydrogenase family.The protein encoded by this gene has both oxidoreductase and epimerase activities and is involved in androgen catabolism. The oxidoreductase activity can convert 3 alpha-adiol to dihydrotestosterone, while the epimerase activity can convert androsterone to epi-androsterone. Both reactions use NAD+ as the preferred cofactor. This gene is a member of the retinol dehydrogenase family. Transcript variants utilizing alternative polyadenylation signals exist.

Supplier: Prosci

NFKB1 (MIM 164011) or NFKB2 (MIM 164012) is bound to REL (MIM 164910), RELA (MIM 164014), or RELB (MIM 604758) to form the NFKB complex. The NFKB complex is inhibited by I-kappa-B proteins (NFKBIA, MIM 164008, or NFKBIB), which inactivate NF-kappa-B by trapping it in the cytoplasm. Phosphorylation of serine residues on the I-kappa-B proteins by kinases (IKBKA, MIM 600664 or IKBKB, MIM 603258) marks them for destruction via the ubiquitination pathway, thereby allowing activation of the NF-kappa-B complex. Activated NFKB complex translocates into the nucleus and binds DNA at kappa-B-binding motifs such as 5-prime GGGRNNYYCC 3-prime or 5-prime HGGARNYYCC 3-prime (where H is A, C, or T; R is an A or G purine; and Y is a C or T pyrimidine).

Supplier: Prosci

THRB is a nuclear hormone receptor for triiodothyronine. It is one of the several receptors for thyroid hormone, and has been shown to mediate the biological activities of thyroid hormone. Knockout studies in mice suggest that the different receptors, while having certain extent of redundancy, may mediate different functions of thyroid hormone. Defects in this gene are known to be a cause of generalized thyroid hormone resistance (GTHR), a syndrome characterized by goiter and high levels of circulating thyroid hormone (T3-T4), with normal or slightly elevated thyroid stimulating hormone (TSH). Several transcript variants have been observed for this gene, but the full-length nature of only one has been determined so far.

Supplier: Biotium

Calgranulin B / MRP-8/-14 Monoclonal antibody, Clone: MAC387, Host: Mouse, Species reactivity: Monkey, Goat, Baboon, Pig, Dog, Cow, Cat, Rat, Human, Isotype: IgG1, K, Conjugate: CF488A, Synonyms: MAC 387 / S100A8/A9 / Macrophage Ag, Size: 100uL

Supplier: Biotium

Calgranulin B / MRP-8/-14 Monoclonal antibody, Clone: MAC387, Host: Mouse, Species reactivity: Monkey, Goat, Baboon, Pig, Dog, Cow, Cat, Rat, Human, Isotype: IgG1, K, Conjugate: CF568, Synonyms: MAC 387 / S100A8/A9 / Macrophage Ag, Size: 500 uL

Supplier: Biotium

TNF alphA, Monoclonal antibody, Clone: TNF656, Host: Mouse, Species reactivity: Human, Isotype: IgG1, kappa, Conjugate: CF405S, Immunogen: Recombinant human TNF-alpha, Application: Immunofluorescence, Flow cytometry, Size: 100uL

Supplier: Bioss

The protein encoded by this gene is a member of the Fe65 protein family. It is an adaptor protein localized in the nucleus. It interacts with the Alzheimer's disease amyloid precursor protein (APP), transcription factor CP2/LSF/LBP1 and the low-density lipoprotein receptor-related protein. APP functions as a cytosolic anchoring site that can prevent the gene product's nuclear translocation. This encoded protein could play an important role in the pathogenesis of Alzheimer's disease. It is thought to regulate transcription. Also it is observed to block cell cycle progression by downregulating thymidylate synthase expression. Multiple alternatively spliced transcript variants encoding different isoforms have been described for this gene.

Supplier: Bioss

The protein encoded by this gene is a member of the Fe65 protein family. It is an adaptor protein localized in the nucleus. It interacts with the Alzheimer's disease amyloid precursor protein (APP), transcription factor CP2/LSF/LBP1 and the low-density lipoprotein receptor-related protein. APP functions as a cytosolic anchoring site that can prevent the gene product's nuclear translocation. This encoded protein could play an important role in the pathogenesis of Alzheimer's disease. It is thought to regulate transcription. Also it is observed to block cell cycle progression by downregulating thymidylate synthase expression. Multiple alternatively spliced transcript variants encoding different isoforms have been described for this gene.

Supplier: Prosci

Mutations in nAChRs are found in a rare form of nocturnal frontal lobe epilepsy. Previously, some nAChR mutations have been described that are associated with additional neurological features such as psychiatric disorders or cognitive defects. A new CHRNB2 mutation located in transmembrane region 3 (M3), outside the known ADNFLE mutation cluster. The CHRNB2 mutation I312M, which occurred de novo in twins, markedly increases the receptor's sensitivity to acetylcholine. Phenotypically, the mutation is associated not only with typical ADNFLE, but also with distinct deficits in memory. The cognitive problems are most obvious in tasks requiring the organization and storage of verbal information.

Supplier: Prosci

Mutations in nAChRs are found in a rare form of nocturnal frontal lobe epilepsy. Previously, some nAChR mutations have been described that are associated with additional neurological features such as psychiatric disorders or cognitive defects. A new CHRNB2 mutation located in transmembrane region 3 (M3), outside the known ADNFLE mutation cluster. The CHRNB2 mutation I312M, which occurred de novo in twins, markedly increases the receptor's sensitivity to acetylcholine. Phenotypically, the mutation is associated not only with typical ADNFLE, but also with distinct deficits in memory. The cognitive problems are most obvious in tasks requiring the organization and storage of verbal information.

Supplier: Bioss

The protein encoded by this gene is a member of the Fe65 protein family. It is an adaptor protein localized in the nucleus. It interacts with the Alzheimer's disease amyloid precursor protein (APP), transcription factor CP2/LSF/LBP1 and the low-density lipoprotein receptor-related protein. APP functions as a cytosolic anchoring site that can prevent the gene product's nuclear translocation. This encoded protein could play an important role in the pathogenesis of Alzheimer's disease. It is thought to regulate transcription. Also it is observed to block cell cycle progression by downregulating thymidylate synthase expression. Multiple alternatively spliced transcript variants encoding different isoforms have been described for this gene. [provided by RefSeq, Mar 2012]

Supplier: Bioss

The protein encoded by this gene is a member of the Fe65 protein family. It is an adaptor protein localized in the nucleus. It interacts with the Alzheimer's disease amyloid precursor protein (APP), transcription factor CP2/LSF/LBP1 and the low-density lipoprotein receptor-related protein. APP functions as a cytosolic anchoring site that can prevent the gene product's nuclear translocation. This encoded protein could play an important role in the pathogenesis of Alzheimer's disease. It is thought to regulate transcription. Also it is observed to block cell cycle progression by downregulating thymidylate synthase expression. Multiple alternatively spliced transcript variants encoding different isoforms have been described for this gene. [provided by RefSeq, Mar 2012]

Supplier: Bioss

The protein encoded by this gene is a member of the Fe65 protein family. It is an adaptor protein localized in the nucleus. It interacts with the Alzheimer's disease amyloid precursor protein (APP), transcription factor CP2/LSF/LBP1 and the low-density lipoprotein receptor-related protein. APP functions as a cytosolic anchoring site that can prevent the gene product's nuclear translocation. This encoded protein could play an important role in the pathogenesis of Alzheimer's disease. It is thought to regulate transcription. Also it is observed to block cell cycle progression by downregulating thymidylate synthase expression. Multiple alternatively spliced transcript variants encoding different isoforms have been described for this gene. [provided by RefSeq, Mar 2012]

Supplier: Bioss

Essential component of the COP9 signalosome complex (CSN), a complex involved in various cellular and developmental processes. The CSN complex is an essential regulator of the ubiquitin (Ubl) conjugation pathway by mediating the deneddylation of the cullin subunits of SCF-type E3 ligase complexes, leading to decrease the Ubl ligase activity of SCF-type complexes such as SCF, CSA or DDB2. The complex is also involved in phosphorylation of p53/TP53, c-jun/JUN, IkappaBalpha/NFKBIA, ITPK1 and IRF8/ICSBP, possibly via its association with CK2 and PKD kinases. CSN-dependent phosphorylation of TP53 and JUN promotes and protects degradation by the Ubl system, respectively. Involved in early stage of neuronal differentiation via its interaction with NIF3L1.

Supplier: Bioss

Essential component of the COP9 signalosome complex (CSN), a complex involved in various cellular and developmental processes. The CSN complex is an essential regulator of the ubiquitin (Ubl) conjugation pathway by mediating the deneddylation of the cullin subunits of SCF-type E3 ligase complexes, leading to decrease the Ubl ligase activity of SCF-type complexes such as SCF, CSA or DDB2. The complex is also involved in phosphorylation of p53/TP53, c-jun/JUN, IkappaBalpha/NFKBIA, ITPK1 and IRF8/ICSBP, possibly via its association with CK2 and PKD kinases. CSN-dependent phosphorylation of TP53 and JUN promotes and protects degradation by the Ubl system, respectively. Involved in early stage of neuronal differentiation via its interaction with NIF3L1.

Supplier: Prosci

CAD Antibody: Apoptosis is related to many diseases and induced by a family of cell death receptors and their ligands. Cell death signals are transduced by death domain containing adapter molecules and members of the caspase family of proteases. These death signals finally cause the degradation of chromosomal DNA by activated DNase. A mouse DNase that causes DNA fragmentation was identified recently and designated CAD (for caspase activated deoxyribonuclease). The human homologue of mouse CAD was more recently identified by two groups independently and termed CPAN and DFF40. Human DFF45 and its mouse homologue ICAD are the inhibitors of CPAN/DFF40 and CAD, respectively. Upon cleavage of DFF45/ICAD by activated caspase, DFF40/CAD is released and activated and eventually causes the degradation of DNA in the nuclei. Activation of CAD/DFF40, which causes DNA degradation, is the hallmark of apoptotic cell death.

Supplier: Proteintech

ERO1LB is an essential oxidoreductase that oxidizes proteins in the endoplasmic reticulum to produce disulfide bonds. It acts by oxidizing directly P4HB/PDI isomerase through a direct disulfide exchange. It does not act as a direct oxidant of folding substrate, but relies on P4HB/PDI to transfer oxidizing equivalent. Associates with ERP44 but not with GRP54, demonstrating that it does not oxidize all PDI related proteins and can discriminate between PDI and related proteins. Its reoxidation probably involves electron transfer to molecular oxygen via FAD. Glutathione may be required to regulate its activity in the endoplasmic reticulum. It may be responsible for a significant proportion of reactive oxygen species (ROS) in the being a source of oxidative stress. It is required for the folding of cell, thereby being a source of oxidative stress. This antibody has no cross reaction to ERO1L.

Supplier: Thermo Scientific

This gene encodes a subunit of interleukin 12, a cytokine that acts on T and natural killer cells, and has a broad array of biological activities. Interleukin 12 is a disulfide-linked heterodimer composed of the 40 kD cytokine receptor like subunit encoded by this gene, and a 35 kD subunit encoded by IL12A. This cytokine is expressed by activated macrophages that serve as an essential inducer of Th1 cells development. This cytokine has been found to be important for sustaining a sufficient number of memory/effector Th1 cells to mediate long-term protection to an intracellular pathogen. Overexpression of this gene was observed in the central nervous system of patients with multiple sclerosis , suggesting a role of this cytokine in the pathogenesis of the disease. The promoter polymorphism of this gene has been reported to be associated with the severity of atopic and non-atopic asthma in children.

Supplier: Bioss

Apoptosis is a cell death process that removes toxic and/or useless cells during mammalian development. The apoptotic process is accompanied by shrinkage and fragmentation of the cells and nuclei and degradation of the chromosomal DNA into nucleosomal units. DNA fragmentation factor (DFF) is a heterodimeric protein of 40-kD (DFFB) and 45-kD (DFFA) subunits. DFFA is the substrate for caspase-3 and triggers DNA fragmentation during apoptosis. DFF becomes activated when DFFA is cleaved by caspase-3. The cleaved fragments of DFFA dissociate from DFFB, the active component of DFF. DFFB has been found to trigger both DNA fragmentation and chromatin condensation during apoptosis. Alternatively spliced transcript variants encoding distinct isoforms have been found for this gene but the biological validity of these variants has not been determined. [provided by RefSeq, Jul 2008].

Supplier: Prosci

CAD Antibody: Apoptosis is related to many diseases and induced by a family of cell death receptors and their ligands. Cell death signals are transduced by death domain containing adapter molecules and members of the caspase family of proteases. These death signals finally cause the degradation of chromosomal DNA by activated DNase. A mouse DNase that causes DNA fragmentation was identified recently and designated CAD (for caspase activated deoxyribonuclease). The human homologue of mouse CAD was more recently identified by two groups independently and termed CPAN and DFF40. Human DFF45 and its mouse homologue ICAD are the inhibitors of CPAN/DFF40 and CAD, respectively. Upon cleavage of DFF45/ICAD by activated caspase, DFF40/CAD is released and activated and eventually causes the degradation of DNA in the nuclei. Activation of CAD/DFF40, which causes DNA degradation, is the hallmark of apoptotic cell death.

Supplier: Enzo Life Sciences

Autophagy is an alternative process of proteasomal degradation for some long-lived proteins or organelles. Alterations in the autophagic-lysosomal compartment have been linked to neuronal death in many neurodegenerative disorders as well as in transmissible neuronal pathologies (prion diseases). Genetic studies in yeast have shown that Autophagy-defective Gene-8 (Atg-8) represents a specific marker for autophagy. Among the four families of mammalian Atg8-related proteins only LC3 (Microtubule-associated Protein1 Light Chain 3) is expressed at sufficient high levels and efficiently recruited to autophagic vesicles in cells and tissues. During autophagy the cytoplasmic form, LC3-I is processed and recruited to autophagosomes, where LC3-II is generated by site specific proteolysis near to the C-terminus. Autophagic vacuoles have been also reported frequently in cardiomyopathies or muscle cells exposed to different experimental settings.

Supplier: Bioss

Apoptosis is a cell death process that removes toxic and/or useless cells during mammalian development. The apoptotic process is accompanied by shrinkage and fragmentation of the cells and nuclei and degradation of the chromosomal DNA into nucleosomal units. DNA fragmentation factor (DFF) is a heterodimeric protein of 40-kD (DFFB) and 45-kD (DFFA) subunits. DFFA is the substrate for caspase-3 and triggers DNA fragmentation during apoptosis. DFF becomes activated when DFFA is cleaved by caspase-3. The cleaved fragments of DFFA dissociate from DFFB, the active component of DFF. DFFB has been found to trigger both DNA fragmentation and chromatin condensation during apoptosis. Alternatively spliced transcript variants encoding distinct isoforms have been found for this gene but the biological validity of these variants has not been determined. [provided by RefSeq, Jul 2008].

Supplier: Prosci

The coatomer is a cytosolic protein complex that binds to dilysine motifs and reversibly associates with Golgi non-clathrin-coated vesicles, which further mediate biosynthetic protein transport from the ER, via the Golgi up to the trans Golgi network. Coatomer complex is required for budding from Golgi membranes, and is essential for the retrograde Golgi-to-ER transport of dilysine-tagged proteins. In mammals, the coatomer can only be recruited by membranes associated to ADP-ribosylation factors (ARFs), which are small GTP-binding proteins; the complex also influences the Golgi structural integrity, as well as the processing, activity, and endocytic recycling of LDL receptors.

Supplier: Enzo Life Sciences

Autophagy is an alternative process of proteasomal degradation for some long-lived proteins or organelles. Alterations in the autophagic-lysosomal compartment have been linked to neuronal death in many neurodegenerative disorders as well as in transmissible neuronal pathologies (prion diseases). Genetic studies in yeast have shown that Autophagy-defective Gene-8 (Atg-8) represents a specific marker for autophagy. Among the four families of mammalian Atg8-related proteins only LC3 (Microtubule-associated Protein1 Light Chain 3) is expressed at sufficient high levels and efficiently recruited to autophagic vesicles in cells and tissues. During autophagy the cytoplasmic form, LC3-I is processed and recruited to autophagosomes, where LC3-II is generated by site specific proteolysis near to the C-terminus. Autophagic vacuoles have been also reported frequently in cardiomyopathies or muscle cells exposed to different experimental settings.

Supplier: Bioss

Apoptosis is a cell death process that removes toxic and/or useless cells during mammalian development. The apoptotic process is accompanied by shrinkage and fragmentation of the cells and nuclei and degradation of the chromosomal DNA into nucleosomal units. DNA fragmentation factor (DFF) is a heterodimeric protein of 40-kD (DFFB) and 45-kD (DFFA) subunits. DFFA is the substrate for caspase-3 and triggers DNA fragmentation during apoptosis. DFF becomes activated when DFFA is cleaved by caspase-3. The cleaved fragments of DFFA dissociate from DFFB, the active component of DFF. DFFB has been found to trigger both DNA fragmentation and chromatin condensation during apoptosis. Alternatively spliced transcript variants encoding distinct isoforms have been found for this gene but the biological validity of these variants has not been determined. [provided by RefSeq, Jul 2008].

Supplier: Biotium

Calgranulin B Monoclonal antibody, Clone: MAC387, Host: Mouse, Species: Monkey, Goat, Baboon, Pig, Dog, Cow, Isotype: IgG1, kappa, Conjugate: CF405S, Immunogen: Recognizes the L1 or Calprotectin of a 12kDa and a 14kDa, Synonyms: S100A8, Application: IF, Fc, Size: 500ul

Supplier: Prosci

CAD Antibody: Apoptosis is related to many diseases and induced by a family of cell death receptors and their ligands. Cell death signals are transduced by death domain containing adapter molecules and members of the caspase family of proteases. These death signals finally cause the degradation of chromosomal DNA by activated DNase. A mouse DNase that causes DNA fragmentation was identified recently and designated CAD (for caspase activated deoxyribonuclease). The human homologue of mouse CAD was more recently identified by two groups independently and termed CPAN and DFF40. Human DFF45 and its mouse homologue ICAD are the inhibitors of CPAN/DFF40 and CAD, respectively. Upon cleavage of DFF45/ICAD by activated caspase, DFF40/CAD is released and activated and eventually causes the degradation of DNA in the nuclei. Activation of CAD/DFF40, which causes DNA degradation, is the hallmark of apoptotic cell death.

Supplier: Proteintech

AP3B1 is the 140-kDa β3A subunit of the adaptor-related protein complex-3 (AP-3), a ubiquitous heterotetrameric complex that is localized to the trans-Golgi network and endosomes and is involved in protein trafficking to lysosomes or specialized endosomal-lysosomal organelles . This complex is composed of two lager subunits (δ and β3A or β3B), a medium subunit (μ3A or μ3B), and a small subunit (σ3A or σ3B). The absence of the β3A subunit (AP3B1) results in the loss of stability of AP3 and leads to degradation of μ3A, to which β3A is directly bound, while the other subunits are variably affected . AP3B1 contains three main domains: the N-terminal head domain, the hinge, and the C-terminal ear domain. It has been reported as a target of IP(7)-mediated pyrophosphorylation . Defects in AP3B1 are the cause of Hermansky-Pudlak syndrome type 2 (HPS2) .

Supplier: Prosci

THRB is a nuclear hormone receptor for triiodothyronine. It is one of the several receptors for thyroid hormone, and has been shown to mediate the biological activities of thyroid hormone. Knockout studies in mice suggest that the different receptors, while having certain extent of redundancy, may mediate different functions of thyroid hormone. Defects in this gene are known to be a cause of generalized thyroid hormone resistance (GTHR), a syndrome characterized by goiter and high levels of circulating thyroid hormone (T3-T4), with normal or slightly elevated thyroid stimulating hormone (TSH). Several transcript variants have been observed for this gene, but the full-length nature of only one has been determined so far.

Supplier: Prosci

ITGB3BP is a transcription coregulator that can have both coactivator and corepressor functions. Isoform 1, but not other isoforms, is involved in the coactivation of nuclear receptors for retinoid X (RXRs) and thyroid hormone (TRs) in a ligand-dependent fashion. ITGB3BP acts as a transcriptional corepressor via its interaction with the NFKB1 NF-kappa-B subunit, possibly by interfering with the transactivation domain of NFKB1. It induces apoptosis in breast cancer cells, but not in other cancer cells, via a caspase-2 mediated pathway that involves mitochondrial membrane permeabilization but does not require other caspases. ITGB3BP may also act as an inhibitor of cyclin A-associated kinase. ITGB3BP may be involved in incorporation of newly synthesized CENPA into centromeres via its interaction with the CENPA-NAC complex.