Other Proteins

SMAD4 is a member of the SMAD family and mediates signaling by the transforming growth factor-beta (TGFβ) superfamily and related ligands (1). TGFβ stimulation leads to phosphorylation and activation of SMAD1, SMAD2 and SMAD3, which form complexes with SMAD4 that accumulate in the nucleus and regulate transcription of target genes. SMAD signaling is negatively regulated by inhibitory SMADs and ubiquitin-mediated processes and proteasomal degradation of SMADs depend on the direct interaction of specific E3 ligases with SMADs. SMAD4 is targeted for degradation by multiple ubiquitin ligases that can simultaneously act on R-SMADs and signaling receptors. Such mechanisms of down-regulation of TGFβ signaling via degradation of SMADs may be critical for proper physiological response to this pathway (2). SMAD4 Protein is ideal for investigators involved in Signaling Proteins, Transcription Proteins, AKT/PKB Pathway, Angiogenesis, Cancer, Cell Cycle, Cellular Stress, ERK/MAPK Pathway, Inflamma

SMAD5 is a member of the SMAD family and mediates signaling by the transforming growth factor-beta (TGFβ) superfamily and related ligands (1). SMAD5 plays a critical role in the signaling pathway by which TGFβ inhibits the proliferation of human hematopoietic progenitor cells. SMAD5 is up-regulated in gastric epithelial cells during the infection of the pathogen Helicobacter pylori and it mediates apoptosis of gastric epithelial cells induced by H. pylori infection (2). In mature human B cells, bone morphogenetic protein 6 (BMP-6) inhibits cell growth and rapidly induces phosphorylation of SMADs 5 and 8. SMAD5 Protein is ideal for investigators involved in Signaling Proteins, Transcription Proteins, AKT/PKB Pathway, Angiogenesis, Cancer, Cell Cycle, Cellular Stress, ERK/MAPK Pathway, Inflammation, JAK/STAT Pathway, JNK/SAPK Pathway, NfkB Pathway, and WNT Signaling research.

SMAD9 or SMAD family member 9 is a member of the SMAD family. SMAD9 transduces signals from TGF-beta family members which regulate growth, differentiation, apoptosis, and development. SMAD9 is activated by bone morphogenetic proteins and it interacts with SMAD4 (1). SMAD9 positively and negatively regulate BMP signaling, respectively. SMAD9, also known as SMAD8 may play a role in both pulmonary hypertension and lung tumorigenesis (2). Mutations in SMAD9 in patient with pulmonary arterial hypertension (PAH) have been identified and this may be involved in the pathogenesis of PAH. SMAD9 Protein is ideal for investigators involved in Signaling Proteins, Transcription Proteins, AKT/PKB Pathway, Angiogenesis, Cancer, Cell Cycle, Cellular Stress, ERK/MAPK Pathway, Inflammation, JAK/STAT Pathway, JNK/SAPK Pathway, NfkB Pathway, and WNT Signaling research.

SMAD9 or SMAD family member 9 is a member of the SMAD family. SMAD9 transduces signals from TGF-beta family members which regulate growth, differentiation, apoptosis, and development. SMAD9 is activated by bone morphogenetic proteins and it interacts with SMAD4 (1). SMAD9 positively and negatively regulate BMP signaling, respectively. SMAD9, also known as SMAD8 may play a role in both pulmonary hypertension and lung tumorigenesis (2). Mutations in SMAD9 in patient with pulmonary arterial hypertension (PAH) have been identified and this may be involved in the pathogenesis of PAH. SMAD9 Protein is ideal for investigators involved in Signaling Proteins, Transcription Proteins, AKT/PKB Pathway, Angiogenesis, Cancer, Cell Cycle, Cellular Stress, ERK/MAPK Pathway, Inflammation, JAK/STAT Pathway, JNK/SAPK Pathway, NfkB Pathway, and WNT Signaling research.

SNCA is a member of the synuclein family which also includes beta- and gamma-synuclein. These proteins are abundantly expressed in the brain and alpha- and beta-synuclein selectively inhibit phospholipase D2 which is a highly conserved protein that is also abundant in neurons, especially presynaptic terminals (1). SNCA gene is not a major risk factor in familial Parkinson disease (2). SNCA may serve to integrate pre-synaptic signaling and membrane trafficking and SNCA peptides are a major component of amyloid plaques in the brains of patients with Alzheimer's disease. SNCA Protein is ideal for investigators involved in Signaling Proteins, Microtubule/Actin Associated Proteins, Cancer, and Neurobiology research.

SNCB is a member of the synuclein family of proteins which are believed to be involved in the pathogenesis of neurodegenerative diseases. SNCB is highly homologous to alpha-synuclein which is abundantly expressed in the brain and putatively inhibits phospholipase D2 selectively. SNCB may play a role in neuronal plasticity, is abundant in neurofibrillary lesions of patients with Alzheimer disease. SNCB is shown to be highly expressed in the substantia nigra of the brain, a region of neuronal degeneration in patients with Parkinson disease but no direct relation to Parkinson disease has been established (1). An alteration in SNCB may impair its normal inhibitory action on the formation of toxic alpha-synuclein fibrils, thereby indirectly contributing to disease pathogenesis (2). SNCB Protein is ideal for investigators involved in Signaling Proteins, Microtubule/Actin Associated Proteins, Cancer, and Neurobiology research.

SNCG or synuclein, gamma (breast cancer-specific protein 1) is a member of the synuclein family of proteins which are believed to be involved in the pathogenesis of neurodegenerative diseases. SNCG gene may also be overexpressed in ovarian cancers (1). The overexpression of SNCG may indicate breast cancer malignant progression from benign or in situ carcinoma. SNCG may also play a role in motor neurons dysfunction and cell death (2). Synuclein proteins play an important role in regulating neurotransmitter release from specific populations of midbrain dopamine neurons through mechanisms that differ from those reported in other neurons. SNCG Protein is ideal for investigators involved in Signaling Proteins, Microtubule/Actin Associated Proteins, Cancer, and Neurobiology research.

SNCG or synuclein, gamma (breast cancer-specific protein 1) is a member of the synuclein family of proteins which are believed to be involved in the pathogenesis of neurodegenerative diseases. SNCG gene may also be overexpressed in ovarian cancers (1). The overexpression of SNCG may indicate breast cancer malignant progression from benign or in situ carcinoma. SNCG may also play a role in motor neurons dysfunction and cell death (2). Synuclein proteins play an important role in regulating neurotransmitter release from specific populations of midbrain dopamine neurons through mechanisms that differ from those reported in other neurons. SNCG Protein is ideal for investigators involved in Signaling Proteins, Microtubule/Actin Associated Proteins, Cancer, and Neurobiology research.

SOD1 (superoxide dismutase 1) is the major soluble cytoplasmic enzyme responsible for destroying harmful free superoxide radicals in the body thereby providing defense against oxygen free-radical toxicity. Soluble cytoplasmic SOD1 is a copper- and zinc-containing enzyme and the SOD1 gene maps to chromosome 21q22 (1). Mutations in the SOD1 gene have been implicated to be the cause of familial amyotrophic lateral sclerosis, increased age-related muscle mass loss, early development of cataracts, macular degeneration, thymic involution, hepatocellular carcinoma, and shortened lifespan (2). SOD1 Protein is ideal for investigators involved in Signaling Proteins, Cell Stress & Chaperone Proteins, Apoptosis/Autophagy, Cancer, Cardiovascular Disease, Cellular Stress, Inflammation, and Neurobiology research.