TY - JOUR
T1 - Use of competitive pcr to monitor expression of the bcl-2. bcl-x. mcl-1. box. bak and bfl-1 genes during the induction of apoptosis in human haematopoietic cell lines
AU - Smith, Christopher A.
AU - Ganderton, Sue K.
AU - Culhane, Aedin C.
AU - Leite, Pedro S.
AU - Williams, Gwyn T.
PY - 1996
Y1 - 1996
N2 - We have developed a competitive PCR system to follow changes in the relative abundance of the major mRNAs encoding Bcl-2, Bel-XL, Bcl-xs, Mcl-1, Bax, Bak and Bfl-1. These proteins are all members of the family of human proteins related to the Ccenorhabditis elegans apoptosis-regulating protein Ced-9. Bcl2 and BC!-XL (and probably also Mcl-1 and Bfl-1) inhibit or delay apoptosis, whereas Bax, Bak and Bcl-xs promote apoptosis. Using this system we have monitored changes in the expression of these genes in three human haematopoietic cell lines following treatments that induce cell death by apoptosis. The human cell lines used were Jurkat (T-cell leukaemia), HL60 (promyelocytic leukaemia) and TF1 (IL-3-dependent erythroleukaemia). The treatments used to induce apoptosis were X-irradiation, treatment with the topoisomerase II-inhibiting chemotherapeutic agent etoposide (VP-16) and cytokine deprivation (IL-3 withdrawal).
AB - We have developed a competitive PCR system to follow changes in the relative abundance of the major mRNAs encoding Bcl-2, Bel-XL, Bcl-xs, Mcl-1, Bax, Bak and Bfl-1. These proteins are all members of the family of human proteins related to the Ccenorhabditis elegans apoptosis-regulating protein Ced-9. Bcl2 and BC!-XL (and probably also Mcl-1 and Bfl-1) inhibit or delay apoptosis, whereas Bax, Bak and Bcl-xs promote apoptosis. Using this system we have monitored changes in the expression of these genes in three human haematopoietic cell lines following treatments that induce cell death by apoptosis. The human cell lines used were Jurkat (T-cell leukaemia), HL60 (promyelocytic leukaemia) and TF1 (IL-3-dependent erythroleukaemia). The treatments used to induce apoptosis were X-irradiation, treatment with the topoisomerase II-inhibiting chemotherapeutic agent etoposide (VP-16) and cytokine deprivation (IL-3 withdrawal).
UR - http://www.scopus.com/inward/record.url?scp=33749164944&partnerID=8YFLogxK
M3 - Article
AN - SCOPUS:33749164944
SN - 0300-5127
VL - 24
SP - 600S
JO - Biochemical Society Transactions
JF - Biochemical Society Transactions
IS - 4
ER -