HBB sirna

HBB siRNA (Rat)

Cat. Num. AAA8212146

• Reactivity: Rat
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: HBB; HBB siRNA (Rat); Hemoglobin subunit beta-1; Beta-1-globin; Hemoglobin beta chain. major-form; Hemoglobin beta-1 chain; HBB sirna

• Host: Synthetic
• Reactivity: Rat
• Specificity: HBB siRNA (Rat) is a target-specific 19-23 nt siRNA oligo duplexes designed to knock down gene expression.
• Purity/Purification: > 97%
• Form/Format: Lyophilized powder
• Sequence Length: 147

• Applicable Applications for HBB sirna: RNA Interference (RNAi)
• Quality Control: Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
• Directions for Use: We recommends transfection with 100 nM siRNA 48 to 72 hours prior to cell lysis. Before resuspending, briefly centrifuge the tube to ensure the lyophilized siRNA is at the bottom of the tube. Resuspend the siRNA oligos to an appropriate concentration with DEPC water. For each vial, suitable for 250 transfections in 24 well plate (20 pmol for each well).
• Components: We offer pre-designed sets of 3 different target-specific siRNA oligo duplexes of rat HBB gene. Each vial contains 5 nmol of lyophilized siRNA. The duplexes can be transfected individually or pooled together to achieve knockdown of the target gene, which is most commonly assessed by qPCR or western blot. Our siRNA oligos are also chemically modified (2'-OMe) at no extra charge for increased stability and enhanced knockdown in vitro and in vivo.
• Preparation and Storage: Shipped at 4 degree C. Store at -20 degree C for one year.

Related Product Information for HBB sirna

siRNA to inhibit HBB expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 17985949
• NCBI GeneID: 24440
• NCBI Accession #: NP_150237.1
• NCBI GenBank Nucleotide #: NM_033234.1
• UniProt Accession #: P02091; P33584
• Molecular Weight: 15,979 Da
• NCBI Official Full Name: hemoglobin subunit beta-1
• NCBI Official Synonym Full Names: hemoglobin, beta
• NCBI Official Symbol: Hbb
• NCBI Protein Information: hemoglobin subunit beta-1
• UniProt Protein Name: Hemoglobin subunit beta-1
• Protein Family: Hemoglobin
• UniProt Gene Name: Hbb
• UniProt Entry Name: HBB1_RAT

NCBI Description

beta-globin chain of hemoglobin, which binds and transports oxygen to peripheral tissues [RGD, Feb 2006]

Uniprot Description

HBB: Involved in oxygen transport from the lung to the various peripheral tissues. Defects in HBB may be a cause of Heinz body anemias (HEIBAN). This is a form of non-spherocytic hemolytic anemia of Dacie type 1. After splenectomy, which has little benefit, basophilic inclusions called Heinz bodies are demonstrable in the erythrocytes. Before splenectomy, diffuse or punctate basophilia may be evident. Most of these cases are probably instances of hemoglobinopathy. The hemoglobin demonstrates heat lability. Heinz bodies are observed also with the Ivemark syndrome (asplenia with cardiovascular anomalies) and with glutathione peroxidase deficiency. Defects in HBB are the cause of beta-thalassemia (B-THAL). A form of thalassemia. Thalassemias are common monogenic diseases occurring mostly in Mediterranean and Southeast Asian populations. The hallmark of beta-thalassemia is an imbalance in globin-chain production in the adult HbA molecule. Absence of beta chain causes beta(0)-thalassemia, while reduced amounts of detectable beta globin causes beta(+)-thalassemia. In the severe forms of beta-thalassemia, the excess alpha globin chains accumulate in the developing erythroid precursors in the marrow. Their deposition leads to a vast increase in erythroid apoptosis that in turn causes ineffective erythropoiesis and severe microcytic hypochromic anemia. Clinically, beta-thalassemia is divided into thalassemia major which is transfusion dependent, thalassemia intermedia (of intermediate severity), and thalassemia minor that is asymptomatic. Defects in HBB are the cause of sickle cell anemia (SKCA); also known as sickle cell disease. Sickle cell anemia is characterized by abnormally shaped red cells resulting in chronic anemia and periodic episodes of pain, serious infections and damage to vital organs. Normal red blood cells are round and flexible and flow easily through blood vessels, but in sickle cell anemia, the abnormal hemoglobin (called Hb S) causes red blood cells to become stiff. They are C-shaped and resembles a sickle. These stiffer red blood cells can led to microvascular occlusion thus cutting off the blood supply to nearby tissues. Defects in HBB are the cause of beta-thalassemia dominant inclusion body type (B-THALIB). An autosomal dominant form of beta thalassemia characterized by moderate anemia, lifelong jaundice, cholelithiasis and splenomegaly, marked morphologic changes in the red cells, erythroid hyperplasia of the bone marrow with increased numbers of multinucleate red cell precursors, and the presence of large inclusion bodies in the normoblasts, both in the marrow and in the peripheral blood after splenectomy. Belongs to the globin family.

Protein type: Carrier

Cellular Component: hemoglobin complex

Molecular Function: iron ion binding; heme binding; hemoglobin alpha binding; oxygen binding; hemoglobin beta binding; oxygen transporter activity

Biological Process: erythrocyte development; glutathione metabolic process; protein heterooligomerization; oxygen transport; hemopoiesis