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  • 总部: 泰国曼谷市巴吞汪区仑披尼分区 普勒吉路齐隆巷5号.
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Alternative titles; symbolsANAMORSINHGNC Approved Gene Symbol: CIAPIN1Cytogenetic location: 16q21 Genomic coordinates (GRCh38): 16:57,428,186-57,447,384 (fro...

Alternative titles; symbols


HGNC Approved Gene Symbol: CIAPIN1

Cytogenetic location: 16q21 Genomic coordinates (GRCh38): 16:57,428,186-57,447,384 (from NCBI)

▼ Description
CIAPIN1 is a cytokine-induced inhibitor of apoptosis with no relation to apoptosis regulatory molecules of the BCL2 (151430) or CASP (see 147678) families. Expression of CIAPIN1 is dependent on growth factor stimulation (Shibayama et al., 2004).

▼ Cloning and Expression
Using expression cloning with an IL3 (147740)-independent subline of an IL3-dependent mouse cell line, Shibayama et al. (2004) obtained a cDNA encoding Ciapin1, which they termed Anamorsin, meaning 'anti-death molecule' in Latin. By searching databases, Shibayama et al. (2004) identified human Anamorsin. The predicted 310-amino acid mouse protein has a calculated molecular mass of 37 kD and contains an N-terminal methyltransferase motif. Human and mouse Anamorsin share 82% amino acid identity. Northern blot analysis of human tissues revealed ubiquitous expression of Anamorsin, with particularly high levels in heart, liver, and pancreas. Immunofluorescence microscopy of mouse cells demonstrated that Anamorsin was localized in the cytoplasm exclusively.

▼ Gene Function
Shibayama et al. (2004) found that expression of Anamorsin in mouse cells conferred resistance to apoptosis caused by IL3 deprivation. Addition of growth factors, such as EPO (133170), SCF (184745), TPO (600044), or IL3, all of which depend on RAS (190020) signaling, induced dose-dependent expression of Anamorsin in mouse cells. Based on these results and their findings in Anamorsin null mice, Shibayama et al. (2004) concluded that Anamorsin is critical in hematopoiesis and in the mediation of cytokine-induced antiapoptosis.

▼ Mapping
Loftus et al. (1999) identified the CIAPIN1 gene on chromosome 16.

▼ Animal Model
Shibayama et al. (2004) generated Anamorsin null mice, all of which died by late gestation due to a hematopoiesis defect in fetal liver. Myeloid, and particularly erythroid, colony formation was disrupted in these mice. Microarray analysis revealed reduced expression of Bclxl (600039) and Jak2 (147796) in fetal liver of Anamorsin null mice.

Tags: 16q21