Signal transduction pathways regulated by mitogen-activated/extracellular response kinase kinase kinase induce cell death.

Mitogen-activated/extracellular response kinase kinase (MEK) kinase (MEKK) is a serine-threonine kinase that regulates sequential protein phosphorylation pathways, leading to the activation of mitogen-activated protein kinases (MAPK), including members of the Jun kinase (JNK)/stress-activated protein kinase (SAPK) family. In Swiss 3T3 and REF52 fibroblasts, activated MEKK induces cell death involving cytoplasmic shrinkage, nuclear condensation, and DNA fragmentation characteristic of apoptosis. Expression of activated MEKK enhanced the apoptotic response to ultraviolet irradiation, indicating that MEKK-regulated pathways sensitize cells to apoptotic stimuli.

Requirement of the adenovirus E1A transformation domain 1 for inhibition of PC12 cell neuronal differentiation.

Expression of the adenovirus early gene E1A inhibits the nerve growth factor (NGF)-induced differentiation of PC12 pheochromocytoma cells. Expression of the 12S form of E1A, which lacks the transcription activation region, also inhibited PC12 cell differentiation in a manner similar to the wild-type gene. Three cellular proteins--the retinoblastoma susceptibility gene product referred to as 105(Rb)-, 107-, and 300-kDa proteins--stably interacted with the different E1A polypeptides.

Fluid movement in the lumen of the rat epididymis: effect of vasectomy and subsequent vasovasostomy.

Intraluminal fluid movement rate was measured in four regions of the rat epididymis. The fastest flow occurred in the proximal caput epididymis (18.5 +/- 3.

On the maintenance of male fertility in the absence of native testosterone secretion: site-directed hormonal therapy in the rat.

A method of direct percutaneous injection of testosterone (T)-laden microspheres directly into the testis was used in an attempt to achieve the maintenance of normal intratesticular T concentrations, spermatogenesis, and fertility. Rats were divided into three groups: (1) sham operated/injection controls; (2) animals receiving 250 micrograms/d gonadotropin-releasing hormone (GnRH)-antagonist; and (3) animals receiving GnRH-antagonist as in group 1 plus 20 mg T-laden microspheres/testis. Treatment periods were 45 and 90 days.