✦ LIBER ✦

Interaction of Adrenomedullin with Calcitonin Receptor in Cultured Human Breast Cancer Cells, T 47D

✍ Scribed by Jyoti Disa; Khoa Dang; K.B Tan; Nambi Aiyar

Book ID: 117409117
Publisher: Elsevier Science
Year: 1998
Tongue: English
Weight: 82 KB
Volume: 19
Category: Article
ISSN: 0196-9781
DOI: 10.1016/s0196-9781(97)00376-8

No coin nor oath required. For personal study only.

📜 SIMILAR VOLUMES

Calcitonin-gene-related-peptide acts on

Calcitonin-gene-related-peptide acts on calcitonin receptors in a human breast cancer cell line ( T 47 D )

✍ H-G Schneider; F Raue; R Ziegler 📂 Article 📅 1987 🏛 Elsevier Science 🌐 English ⚖ 142 KB

Progestin regulation of EGF-receptor mRN

Progestin regulation of EGF-receptor mRNA accumulation in T-47D human breast cancer cells

✍ Leigh C Murphy; Liam J Murphy; Robert P.C. Shiu 📂 Article 📅 1988 🏛 Elsevier Science 🌐 English ⚖ 933 KB

Identification of leptin receptors in hu

Identification of leptin receptors in human breast cancer: functional activity in the T47-D breast cancer cell line

✍ K. Laud; I. Gourdou; L. Pessemesse; J.P. Peyrat; J. Djiane 📂 Article 📅 2002 🏛 Elsevier Science 🌐 English ⚖ 259 KB

Adrenomedullin and calcitonin gene-relat

Adrenomedullin and calcitonin gene-related peptide interact with the same receptor in cultured human neuroblastoma SK-N-MC cells

✍ Urs Zimmermann; Jan A. Fischer; Roman Muff 📂 Article 📅 1995 🏛 Elsevier Science 🌐 English ⚖ 508 KB

Short- and long-term estrogen deprivatio

Short- and long-term estrogen deprivation of T47D human breast cancer cells in culture

✍ Murphy, Catherine S.; Meisner, Lorraine F.; Wu, Shi Qi; Craig Jordan, V. 📂 Article 📅 1989 🏛 Elsevier Science ⚖ 746 KB

Interaction of growth factors during pro

Interaction of growth factors during progression towards steroid independence in T-47-D human breast cancer cells

✍ Roger J. Daly; Roger J. B. King; Philippa D. Darbre 📂 Article 📅 1990 🏛 John Wiley and Sons 🌐 English ⚖ 874 KB

When deprived of steroid in the long term, T-47-D human breast cancer cells lose estrogen sensitivity of cell growth. This loss of response results from an increased basal growth rate in the absence of steroid, not from a loss of estrogen-stimulated growth, and it occurs without any loss of estrogen