(PDF) Interleukin-1 and Tumor Necrosis Factor Receptor

Interleukin-1 and Tumor Necrosis Factor Receptor Signaling Is Not Required for Bacteria-Induced Osteoclastogenesis and Bone Loss but Is Essential for Protecting the Host From a Mixed Anaerobic Infection

American Journal of Pathology - United States

doi 10.1016/s0002-9440(10)65532-0

Full Text

Open PDF

Abstract

Available in full text

Date

December 1, 1999

Authors

Publisher

Elsevier BV

Related search

Acid Ceramidase but Not Acid Sphingomyelinase Is Required for Tumor Necrosis Factor-Α-Induced PGE2Production

Journal of Biological Chemistry

English

The Death Domain of Tumor Necrosis Factor Receptor 1 Is Necessary but Not Sufficient for Golgi Retention in Endothelial Cells

English

Fas Receptor Is Required for Estrogen Deficiency-Induced Bone Loss in Mice

Laboratory Investigation

English

NF-κB Activation Is Required for Human Endothelial Survival During Exposure to Tumor Necrosis Factor-Α but Not to Interleukin-1β or Lipopolysaccharide

Journal of Biological Chemistry

English

Lipopolysaccharide-Stimulated Osteoclastogenesis Is Mediated by Tumor Necrosis Factor via Its P55 Receptor.

Journal of Clinical Investigation

Medicine

1997

English

Central Interleukin-1 (IL1) Signaling Is Required for Pharmacological, but Not Physiological, Effects of Leptin on Energy Balance

Brain Research

Neuroscience

Neurology

Developmental Biology

Molecular Biology

2007

English

Tumor Necrosis Factor-Α (TNF) Stimulates RANKL-induced Osteoclastogenesis via Coupling of TNF Type 1 Receptor and RANK Signaling Pathways

Journal of Biological Chemistry

English

Protein Tyrosine Kinase P56lckIs Required for Ceramide-Induced but Not Tumor Necrosis Factor-Induced Activation of NF-κB, AP-1, JNK, and Apoptosis

Journal of Biological Chemistry

English

The Receptor for Interleukin 3 Is Selectively Induced in Human Endothelial Cells by Tumor Necrosis Factor Alpha and Potentiates Interleukin 8 Secretion and Neutrophil Transmigration.

Proceedings of the National Academy of Sciences of the United States of America

Multidisciplinary

1993

English

Amanote Research

Interleukin-1 and Tumor Necrosis Factor Receptor Signaling Is Not Required for Bacteria-Induced Osteoclastogenesis and Bone Loss but Is Essential for Protecting the Host From a Mixed Anaerobic Infection

American Journal of Pathology - United States

doi 10.1016/s0002-9440(10)65532-0

Full Text

Abstract

Categories

Date

Authors

Publisher

Related search

Acid Ceramidase but Not Acid Sphingomyelinase Is Required for Tumor Necrosis Factor-Α-Induced PGE2Production

The Death Domain of Tumor Necrosis Factor Receptor 1 Is Necessary but Not Sufficient for Golgi Retention in Endothelial Cells

Fas Receptor Is Required for Estrogen Deficiency-Induced Bone Loss in Mice

NF-κB Activation Is Required for Human Endothelial Survival During Exposure to Tumor Necrosis Factor-Α but Not to Interleukin-1β or Lipopolysaccharide

Lipopolysaccharide-Stimulated Osteoclastogenesis Is Mediated by Tumor Necrosis Factor via Its P55 Receptor.

Central Interleukin-1 (IL1) Signaling Is Required for Pharmacological, but Not Physiological, Effects of Leptin on Energy Balance

Tumor Necrosis Factor-Α (TNF) Stimulates RANKL-induced Osteoclastogenesis via Coupling of TNF Type 1 Receptor and RANK Signaling Pathways

Protein Tyrosine Kinase P56lckIs Required for Ceramide-Induced but Not Tumor Necrosis Factor-Induced Activation of NF-κB, AP-1, JNK, and Apoptosis

The Receptor for Interleukin 3 Is Selectively Induced in Human Endothelial Cells by Tumor Necrosis Factor Alpha and Potentiates Interleukin 8 Secretion and Neutrophil Transmigration.