目录号 | 产品详情 | 靶点 | |
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T0768L | |||
Oxolamine hydrochloride is a cough suppressant which may be useful in the treatment of pediatric asthma. | |||
T31404 | |||
Dextranomer, for treatment of burns; consists of three-dimensional network of dextran polymers cross-linked by epichlorohydrin; dextranomer based implants usedas a bulking agent for endoscopic treatment of pediatric structural incontinence; ingredient of |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-05242 | CRLF2/TSLPR Protein, Human, Recombinant (His) | Human | HEK293 | ||
Overexpression of cytokine receptor-like factor 2 (CRLF2) due to chromosomal rearrangement has been observed in acute lymphoblastic leukemia (ALL) and reported to contribute to oncogenesis and unfavorable outcome in ALL. The high CRLF2 expression works with the IKZF1 deletion to drive oncogenesis of ALL and has significance in an integrated prognostic model for adult high-risk ALL. Thymic stromal lymphopoietin (TSLP) stimulates in-vitro proliferation of human fetal B-cell precursors. However, its in-vivo role during normal human B lymphopoiesis is unknown. Genetic alterations that cause overexpression of its receptor component, cytokine receptor-like factor 2 (CRLF2), lead to high-risk B-cell acute lymphoblastic leukemia implicating this signaling pathway in leukemogenesis. CRLF2 over-expression is a poor prognostic marker identifying a subset of HR T-ALL patients that could benefit from alternative therapy, potentially targeting the CRLF2 pathway. Cytokine receptor-like factor 2 ( CRLF2 ) rearrangement is found in approximately 50% of pediatric Ph-like B-cell acute lymphoblastic leukemia (B-ALL), and around 50% of CRLF2 + cases harbor JAK mutations. Cytokine receptor-like factor 2(CRLF2) plays an important role in the development of normal B lymphocytes, which can mediate early B cell proliferation and survival.
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TMPY-00518 | SBDS Protein, Human, Recombinant (His) | Human | E. coli | ||
The mutation of Shwachman-Bodian-Diamond syndrome (SBDS) gene has been proposed to be a major causative reason for SDS. Shwachman-Diamond syndrome (SDS) is a rare pediatric disease characterized by various systemic disorders, including hematopoietic dysfunction. SBDS deficiency leads to telomere shortening, that SBDS is a telomere-protecting protein that participates in regulating telomerase recruitment.
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TMPJ-00623 | BAFF/TNFSF13B Protein, Rhesus macaque, Recombinant (hFc) | Rhesus Macaque | Human Cells | ||
TNFSF13B is also known as B-cell activating factor (BAFF), BLyS and TNLG7A, is a member of TNF ligand superfamily. TNFSF/TNFRSF members function as key molecules in local and systemic inflammatory network, and the plasma TNFSF13B and TNFSF14 may be the potential local and systemic inflammatory indicators of severe HAdV pneumonia in pediatric patients. Identification of TNFSF13B as candidate causative genes supports conjectures on involvement of the immune system in BVVL and amyotrophic lateral sclerosis. It’s reported that APRIL, BAFF, and BAFF receptors play a major role in the pathogenesis of RA, and MSCT seems to inhibit these immunological factors.
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TMPY-00452 | SBDS Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
The mutation of Shwachman-Bodian-Diamond syndrome (SBDS) gene has been proposed to be a major causative reason for SDS. Shwachman-Diamond syndrome (SDS) is a rare pediatric disease characterized by various systemic disorders, including hematopoietic dysfunction. SBDS deficiency leads to telomere shortening, that SBDS is a telomere-protecting protein that participates in regulating telomerase recruitment.
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TMPY-05769 | CRLF2/TSLPR Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Overexpression of cytokine receptor-like factor 2 (CRLF2) due to chromosomal rearrangement has been observed in acute lymphoblastic leukemia (ALL) and reported to contribute to oncogenesis and unfavorable outcome in ALL. The high CRLF2 expression works with the IKZF1 deletion to drive oncogenesis of ALL and has significance in an integrated prognostic model for adult high-risk ALL. Thymic stromal lymphopoietin (TSLP) stimulates in-vitro proliferation of human fetal B-cell precursors. However, its in-vivo role during normal human B lymphopoiesis is unknown. Genetic alterations that cause overexpression of its receptor component, cytokine receptor-like factor 2 (CRLF2), lead to high-risk B-cell acute lymphoblastic leukemia implicating this signaling pathway in leukemogenesis. CRLF2 over-expression is a poor prognostic marker identifying a subset of HR T-ALL patients that could benefit from alternative therapy, potentially targeting the CRLF2 pathway. Cytokine receptor-like factor 2 ( CRLF2 ) rearrangement is found in approximately 50% of pediatric Ph-like B-cell acute lymphoblastic leukemia (B-ALL), and around 50% of CRLF2 + cases harbor JAK mutations. Cytokine receptor-like factor 2(CRLF2) plays an important role in the development of normal B lymphocytes, which can mediate early B cell proliferation and survival.
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