Baculoviral IAP Repeat Containing Protein 5 review: Survivin inhibits caspase

Posted by Deeksha on September 20th, 2019

Baculovirus inhibitor of apoptosis protein Repeat (BIR) is known as the structural motif available in proteins having a role in apoptosis, segregation of chromosome and cytokine production. BIR-containing proteins (BIRCs) include BIRC1, BIRC2, BIRC3, BIRC4, BIRC5 and BIRC6. These BIR domains are a part of zinc-finger domain family and possess numerous invariant amino acid residues. Baculoviral IAP Repeat Containing 5 (BIRC 5) is a coding gene and belongs to the gene family inhibitor of apoptosis (IAP). This gene family encodes Survivin, a protein specialized in prevention of apoptotic cell death. BIRC5 gene directs Chromosome passage protein complex (CPC) to various locations during metaphase and cytokinesis, participating in the organization of center spindle. It also recruits CPC to centromeres during early phase of mitosis. BIRC 5 is considered to be multitasking for it performs dual role of preventing apoptosis and promoting cell proliferation. These insights stated are according to an intelligence report, titled, “Baculoviral IAP Repeat Containing Protein 5-Pipeline Review, H2 2019” which has been lately added to Market Research Hub’s (MRH) over-arching repository.

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Survivin protein expressed only in G2-M phase

Survivin protein inhibits caspase activation resulting in programmed cell death or negative regulation of apoptosis. Fetal tissue and most human tumors are highly involved in expressing survivin whereas terminally differentiated cells have no trace. Cell cycle highly regulates expression of Survivin only in the G2-M phase the expression takes place.

Vulvar Intraepithelial Neoplasia and Childhood Malignant Schwannoma are few of the diseases associated with Baculoviral IAP Repeat Containing 5 (BIRC 5).

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Baculoviral IAP Repeat Containing Protein 5 pipeline review: Report Synopsis

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Baculoviral IAP Repeat Containing Protein 5 pipeline review: Research Methodology

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Deeksha

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Deeksha
Joined: January 3rd, 2019
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